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Online FirstList of IssuesDocument Types
Mechanism of Shaoyaotang in Ameliorating Colitis-associated Carcinogenesis in Mice via Modulating AMPK/NF-κB/HIF-1α Signaling Pathway AI Introduction
Abstract：ObjectiveTo investigate the mechanism of Shaoyaotang on tumor formation in colitis-associated carcinogenesis （CAC） mouse models through both in vivo and in vitro experiments， focusing on the AMP-activated protein kinase （AMPK）/nuclear factor-κB （NF-κB）/hypoxia-inducible factor-1α （HIF-1α） signaling pathway.MethodsA chronic CAC mouse model was established by azoxymethane （AOM）/dextran sodium sulfate （DSS）. For the in vivo experiment， the model mice were randomly divided into a normal group， a Shaoyaotang （7.12 g·kg-1） control group， a model group， Shaoyaotang low （3.56 g·kg-1）， medium （7.12 g·kg-1）， and high （14.24 g·kg-1） dosage groups， and a sulfasalazine （0.52 g·kg-1， SASP） group， with 10 mice in each group. After 14 weeks of medication， mice were observed for body weight， disease activity index （DAI） score， colon length， number and size of tumors， the distribution level of proliferating cell nuclear antigen （Ki-67）-positive cells in mice colon by immunohistochemistry （IHC）， p-AMPK， AMPK， p-NF-κB， NF-κB， and HIF-1α protein expression levels by Western blot， alongside serum tumor necrosis factor α （TNF-α） and interleukin-6 （IL-6） levels by enzyme-linked immunosorbent assay （ELISA）. For in vitro analysis， an HT29 colorectal cancer cell culture system was established. Then， the optimal dose of Shaoyaotang-containing serum was determined via the cell counting kit-8 （CCK-8） assay. The serum was divided into a blank group， a Shaoyaotang-containing serum group， Shaoyaotang+AICAR group， Shaoyaotang+Compound C， and Shaoyaotang+BAY group. Finally， p-AMPK， AMPK， p-NF-κB， NF-κB， and HIF-1α protein expression levels in the serum were detected by Western blot.ResultsCompared with the normal group， the model group exhibited significantly decreased body weight， increased DAI score （P<0.01）， significantly shortened colon length， significantly increased number of colon tumors （P<0.01）， significantly increased Ki-67-positive expression in colon tissue （P<0.01）， significantly decreased p-AMPK/AMPK protein expression level， increased p-NF-κB/NF-κB and HIF-1α （P<0.05， P<0.01）， alongside significantly increased serum TNF-α and IL-6 levels （P<0.01）. Compared with the model group， Shaoyaotang groups at each dose showed gradually increased body mass （P<0.05， P<0.01）， reduced DAI scores （in the Shaoyaotang medium group and the Shaoyaotang high group） （P<0.05， P<0.01）， significantly inhibited colon shortening to varying degrees （P<0.05， P<0.01）， significantly decreased the number of colon tumors （P<0.01）， inhibitory effect on colon tumors with diameter <4 mm （in the Shaoyaotang medium group and the Shaoyaotang high group） （P<0.01）， significantly decreased Ki-67-positive expression in colorectal tissues （P<0.05， P<0.01）， a dose-dependent up-regulation of p-AMPK/AMPK protein expression levels （P<0.05， P<0.01）， significantly down-regulated p-NF-κB/NF-κB （P<0.01） and HIF-1α （P<0.01）， alongside decreased TNF-α and IL-6 （in the Shaoyaotang high group） （P<0.01）. The CCK-8 results indicated the highest inhibition rate of HT29 cell proliferation in serum containing 15% Shaoyaotang. Compared with the blank group， the Shaoyaotang group and the Shaoyaotang+AICAR group demonstrated elevated p-AMPK/AMPK protein expression （P<0.01）， as well as significantly decreased p-NF-κB/NF-κB and HIF-1α protein expression （P<0.01）， while the Shaoyaotang+BAY group showed elevated p-AMPK/AMPK protein expression （P<0.01） and significantly decreased p-NF-κB/NF-κB expression （P<0.01）. Compared to the Shaoyaotang group， the Shaoyaotang+Compound C group exhibited significantly decreased p-AMPK/AMPK expression （P<0.01）， while the Shaoyaotang+BAY group demonstrated significantly decreased p-NF-κB/NF-κB protein expression （P<0.05） and significantly elevated HIF-1α protein expression （P<0.05）.ConclusionShaoyaotang ameliorates colonic inflammation and tumor formation in CAC mice， with potential mechanisms relevant to the AMPK/NF-κB/HIF-1α signaling pathway modulation.Keywords：colitis-associated carcinogenesis;Shaoyaotang;AMP-activated protein kinase （AMPK）;nuclear factor-κB （NF-κB）;hypoxia-inducible factor-1α （HIF-1α）355|492|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Zuoguiwan Inhibit Bone Resorption in Ovariectomized Rats via STING/TBK1/NF-κB Signaling Pathway AI Introduction
Abstract：ObjectiveTo investigate the effects of Zuoguiwan on bone resorption in ovariectomized rats and decipher the mechanism based on the stimulator of interferon genes （STING）/TANK-binding kinase 1 （TBK1）/nuclear factor-κB （NF-κB） signaling pathway.MethodsSixty female SD rats were randomly allocated into six groups. Among them， 4 groups underwent bilateral ovariectomies for the modeling of postmenopausal osteoporosis （PMOP）. After the operation， the rats were respectively administrated with distilled water （OVX group）， Bujiale （9·10-5 g·kg-1， BJL group）， low-dose Zuoguiwan （4.725 g·kg-1， ZGWL group）， and high-dose Zuoguiwan （9.45 g·kg-1， ZGWH group）， respectively， through gavage. One group underwent sham surgery with distilled water gavage （Sham）， and one group was taken as the blank control （Blank group）. After 12 weeks of gavage， rat serum， femurs， and bone marrow were collected for indicator measurement. Micro CT was used to analyze distal femoral bone parameters and bone tissue microstructure. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the serum levels of cross-linked carboxy-terminal telopeptide of type Ⅰ collagen （CTX-Ⅰ） and tartrate-resistant acid phosphatase 5b （TRACP-5b）， as well as the bone marrow levels of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）. Western blot was employed to quantify the expression levels of bone resorption-related proteins receptor activator of nuclear factor-κB ligand （RANKL）， tartrate-resistant acid phosphatase （TRAP）， and osteoprotegerin （OPG） in the bone marrow tissue， as well as STING/TBK1/NF-κB pathway-related proteins STING， TBK1， NF-κB p65， and p-NF-κB p65.ResultsCompared with the sham group， the OVX group exhibited reduced femoral bone mineral density， cortical bone thickness， trabecular volume fraction， trabecular thickness， and trabecular connection density （P<0.01）， as well as increased trabecular separation （P<0.01）， which indicated disruption of the bone microstructure. Additionally， the OVX group showed elevated serum levels of CTX-Ⅰ and TRACP-5b （P<0.01） and bone marrow levels of IL-1β and TNF-α （P<0.01）， up-regulated protein levels of RANKL， TRAP， STING， and TBK1 and phosphorylation level of NF-κB p65 in the bone marrow （P<0.01）， and down-regulated protein level of OPG （P<0.01）. Compared with the OVX group， the BJL group and the ZGWH group restored the aforementioned indicators to different degrees （P<0.05， P<0.01）.ConclusionZuoguiwan reduce the expression levels of inflammatory cytokines in the bone marrow to inhibit bone resorption by suppressing the activation of the STING/TBK1/NF-κB signaling pathway， thereby significantly improving bone metabolism parameters and bone tissue microarchitecture.Keywords：Zuoguiwan;postmenopausal osteoporosis;bone resorption;stimulator of interferon genes （STING）/TANK-binding kinase 1 （TBK1）/nuclear factor-κB （NF-κB） signaling pathway;bone immunity232|475|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Mechanism of Action of Shenghui Tang Ameliorating Synaptic Plasticity and Cognitive Dysfunction of Zebrafish Models with Alzheimer's Disease via Regulating cAMP/PKA/CREB/BDNF Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveThis paper aims to investigate the ameliorative effect of Shenghui Tang on learning and memory impairment in aluminum chloride （AlCl3）-induced zebrafish models with Alzheimer's disease （AD） and explore its molecular mechanisms， with a focus on its regulatory effects on the cyclic adenosine monophosphate （cAMP）/protein kinase A （PKA）/cAMP response element-binding protein （CREB）/brain-derived neurotrophic factor （BDNF） signaling pathway and synaptic plasticity.MethodsBy using a random number table， a total of 150 wild-type AB strain zebrafish （aged 6-7 months） were divided into a blank group， a model group， Shenghui Tang groups with low， middle， and high doses （0.74， 1.48， and 2.96 g·kg-1）， and a donepezil group （0.01 g·kg-1）. The AD model was established via the chronic AlCl3 immersion method （0.000 2 g·kg-1） for 30 days. T-maze test was used to assess spatial learning and memory of zebrafish. The novel object recognition test was used to detect recognition memory of zebrafish. Anxiety-like behavior of zebrafish was assessed by the novel tank diving test. Telencephalic neuronal morphology was observed by hematoxylin-eosin （HE） staining. Fluoro-Jade B （FJB） staining was applied for degenerative neurons in the telencephalon. Transmission electron microscope （TEM） was used for synaptic ultrastructure in the telencephalon. Enzyme-linked immunosorbent assay （ELISA） was used to detect the content of cAMP in the brain tissue. Western blot was used to analyze the protein expression levels of PKA， CREB， phosphorylated （p）-CREB， BDNF， synaptophysin （SYN）， and postsynaptic density protein-95 （PSD-95） in the brain tissue. Real-time polymerase chain reaction （Real-time PCR） was used to detect the mRNA levels of PKA， CREB， and BDNF， as well as apoptosis-related genes B cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and cysteine-aspartic protease 3 （Caspase-3）.ResultsCompared with the blank group， the model group exhibited prolonged latency to first entry into the EC zone （P<0.01）， reduced entries into the EC zone （P<0.01）， significantly decreased novel object recognition index （P<0.01）， significantly increased latency to first entry into the top zone （P<0.01）， and reduced residence time in the top zone （P<0.01）. The number of degenerative neurons in the telencephalon was significantly increased （P<0.01）. The model group expressed disordered neuronal arrangement， soma atrophy， nuclear pyknosis， and cytoplasmic vacuolation. Mitochondrial cristae membrane exhibited rupture， swelling， and vacuolation. The Bcl-2 mRNA level was downregulated （P<0.01）， and Bax and Caspase-3 levels were upregulated （P<0.01）. Reduced number of presynaptic vesicles， widened synaptic cleft， and thinned postsynaptic density were observed. The expression of synapse-related proteins SYN and PSD-95 was significantly decreased （P<0.01）. The cAMP content was decreased in the brain tissue （P<0.01）. The protein expression levels of PKA， CREB， p-CREB， and BDNF were significantly reduced （P<0.01）， and the mRNA expression levels of PKA， CREB， and BDNF were significantly downregulated （P<0.01）. Compared with the model group， Shenghui Tang groups with middle and high doses and donepezil group showed improved learning and memory ability and anxiety-like behavior， characterized by shortened latency to first entry into the EC zone （P<0.01）， increased number of crossings into the EC zone （P<0.01）， elevated novel object recognition index （P<0.01）， reduced latency to first entry into the top zone， and longer residence time in the top zone （P<0.01）. The number of degenerative neurons in the telencephalon of each treatment group was reduced （P<0.01）， with improved neuronal morphology and relatively regular arrangement， as well as decreased nuclear pyknosis and vacuolation. Mitochondrial cristae membrane integrity was improved， and vacuolation was reduced. The Shenghui Tang groups with middle and high doses exhibited upregulated mRNA expression of Bcl-2 （P<0.01） and downregulated mRNA expression of Bax and Caspase-3 （P<0.05，P<0.05）. In each treatment group， the number of synaptic vesicles increased， and the synaptic cleft narrowed. The postsynaptic density thickened， and the expression of synaptic-related proteins SYN and PSD-95 was enhanced. In Shenghui Tang groups with different doses， cAMP content was increased （P<0.01）， and the mRNA levels of PKA and CREB were upregulated （P<0.01）. Specifically， the mRNA level of BDNF was upregulated in Shenghui Tang groups with medium and high doses （P<0.05，P<0.01）. The donepezil group showed upregulated mRNA expression levels of PKA and CREB （P<0.01）. In the Shenghui Tang groups with medium and high doses， the protein expression levels of PKA， CREB， p-CREB， and BDNF were all significantly increased （P<0.01）， and the protein expression levels of p-CREB and BDNF were increased in the Shenghui Tang groups with low dose （P<0.01）. In the donepezil group， the protein expression of CREB， p-CREB， and BDNF was significantly enhanced （P<0.01）.ConclusionShenghui Tang alleviates learning and memory impairment and anxiety-like behaviors in AlCl3-induced AD zebrafish by activating the cAMP/PKA/CREB/BDNF signaling pathway to improve synaptic plasticity and inhibit neuronal apoptosis.Keywords：Shenghui Tang;Alzheimer's disease;zebrafish;learning and memory;cyclic adenosine monophosphate （cAMP）/protein kinase A （PKA）/cAMP response element-binding protein （CREB）/brain-derived neurotrophic factor （BDNF） signaling pathway;synaptic plasticity247|119|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Xuefu Zhuyutang Treats Coronary Heart Disease with Blood Stasis Syndrome in Rats via SIRT3 Signaling Pathway-mediated Regulation of Endothelial Function Enhanced Publication AI Introduction
Abstract：ObjectiveTo explore the mechanism of action of silent information regulator 3 （SIRT3） in the repair of myocardial and endothelial functions in the rat model of coronary heart disease （CHD） with blood stasis syndrome， as well as the intervention effect of Xuefu Zhuyutang.MethodsA total of 90 specific pathogen-free （SPF） male Sprague-Dawley （SD） rats were used. After model establishment， 16 rats died， and the survived 74 were randomly assigned into seven groups： normal （n=10）， sham （thread passed without ligation， n=10）， model （n=10）， diltiazem （16 mg·kg-1， n=11）， and low-， medium-， and high-dose Xuefu Zhuyutang （3.51， 7.02， and 14.04 g·kg-1， respectively， n=11 each）. The CHD model with blood stasis syndrome was induced by ligation of the left anterior descending （LAD） coronary artery， followed by 7 days of treatment. Rats were then evaluated in terms of general conditions， electrocardiogram （ECG）， cardiac color Doppler ultrasonography （echocardiography， Echo）， and hemorheology. Myocardial histopathology was examined by hematoxylin-eosin （HE） staining. The serum level of nitric oxide （NO） was measured by colorimetry， and inducible nitric oxide synthase （iNOS）， endothelial nitric oxide synthase （eNOS）， and endothelin-1 （ET-1） levels were determined by enzyme-linked immunosorbent assay （ELISA）. Immunohistochemistry （IHC） was employed to assess the expression of hypoxia-inducible factor-1α （HIF-1α） and 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3） in the myocardial tissue. Western blot and Real-time polymerase chain reaction （Real-time PCR） were employed to measure the protein and mRNA levels， respectively， of SIRT3， peroxisome proliferator-activated receptor γ （PPARγ）， and β-catenin.ResultsCompared with the normal group， the model group exhibited poor general conditions and blood stasis syndrome. HE staining showed disorganized cardiomyocytes， partial myofiber rupture and degeneration， nuclear pyknosis or loss， interstitial edema， and extensive neutrophil infiltration in the model group. ECG revealed persistent ST-segment elevation， abnormal Q waves in some rats， reduced R-wave amplitude， irregular R-R intervals， and tall or inverted T waves in the model group. Furthermore， the model group showed decreased left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01）， increased left ventricular end-diastolic dimension （LVIDd） and left ventricular end-systolic dimension （LVIDs） （P<0.01）， elevated whole-blood viscosity at low， medium， and high shear rates， plasma viscosity， and fibrinogen （P<0.01）， declined serum levels of NO and eNOS （P<0.01）， raised serum levels of iNOS and ET-1 （P<0.01）， upregulated protein levels of HIF-1α and PFKFB3 （P<0.01）， downregulated protein and mRNA levels of SIRT3 and PPARγ， and upregulated protein and mRNA levels of β-catenin （P<0.01） in the myocardial tissue. Compared with the model group， medium- and high-dose Xuefu Zhuyutang improved general conditions and ECG， reduced the myocardial damage and inflammation， decreased the LVIDd and whole-blood viscosity at low shear rate （P<0.01）， elevated the serum level of eNOS and reduced the serum level of iNOS （P<0.01）， upregulated the protein level of PFKFB3 and the protein and mRNA levels of SIRT3 and PPARγ （P<0.01）， and downregulated the protein level of β-catenin （P<0.01） in the myocardial tissue. The low-， medium-， and high-dose Xuefu Zhuyutang groups showed increased LVEF and LVFS （P<0.05， P<0.01）， decreased LVIDs， whole-blood viscosity at medium and high shear rates， plasma viscosity， and fibrinogen （P<0.01）， elevated serum level of NO （P<0.01）， declined serum level of ET-1 （P<0.01）， upregulated protein level of HIF-1α （P<0.05， P<0.01） and downregulated mRNA level of β-catenin （P<0.01） in the myocardial tissue.ConclusionXuefu Zhuyutang may promote myocardial repair and functional improvement in the rat model of coronary heart disease with blood stasis syndrome by activating the SIRT3 signaling pathway， coordinately regulating the expression of key proteins such as HIF-1α， PFKFB3， PPARγ， and β-catenin， and modulating endothelial function through multiple aspects including metabolic homeostasis， cell junction stability， and vascular tone coordination.Keywords：coronary heart disease;blood stasis syndrome;Xuefu Zhuyutang;silent information regulator 3 （SIRT3）;endothelial function131|98|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Investigating Therapeutic Efficacy and Mechanisms of Huangliantang on Reflux Esophagitis Based on Esophageal Microbiota Enhanced Publication AI Introduction
Abstract：ObjectiveTo explore the therapeutic effect of Huangliantang on reflux esophagitis in rats based on the esophageal microbiota-bile acid metabolism.MethodsA reflux esophagitis model was established through the forestomach ligation+pyloric clip-induced incomplete pyloric obstruction method. Rats were assigned into sham operation （control）， model， high-dose （51.54 g·kg-1）， medium-dose （25.77 g·kg-1）， and low-dose （12.885 g·kg-1） Huangliantang， and positive drug （omeprazole enteric-coated tablets， 5 mg·kg-1） groups， with 10 rats in each group. After 2 weeks of continuous administration， hematoxylin-eosin （HE） staining was performed to observe histopathological changes in the esophageal tissue， and 16S rRNA high-throughput sequencing was employed to detect changes in the esophageal microbiota. Targeted metabolomics was employed to measure the bile acid levels. Enzyme-linked immunosorbent assay kits were used to determine the key serum inflammatory markers， gastrointestinal hormones， and functional indicators.ResultsHistopathological results showed significant squamous epithelial cell hyperplasia and papillary projections in the lamina propria of the model group， which were markedly alleviated after drug intervention. Compared with the control group， the model group exhibited elevated serum levels of interleukin （IL）-1β and tumor necrosis factor （TNF）-α （P<0.05， P<0.01） and declined level of IL-10 （P<0.01）. Compared with the model group， all drug intervention groups reduced the serum levels of IL-1β and TNF-α （P<0.05， P<0.01） and increased the IL-10 levels （P<0.01）， with the high-dose group showing the most pronounced effects. Additionally， compared with the control group， the model group elevated the serum levels of motilin （P<0.01）， gastrin （P<0.01）， substance P （P<0.01）， vasoactive intestinal peptide （P<0.01）， pepsin （P<0.01）， and pepsinogen （P<0.01）. Drug intervention ameliorated gastrointestinal dysfunction and reduced serum levels of gastrointestinal hormones and functional indicators （P<0.05， P<0.01）. Esophageal microbiota data revealed a significant reduction in the abundance of esophageal microbiota in the model group compared with the control group. Huangliantang intervention significantly increased the abundance， especially that of Lactobacillus species （Lactobacillus johnsonii、Ligilactobacillus murinus、Lactobacillus intestinalis）， and reduced the abundance of harmful bacteria （e.g.， Lachnospiraceae， Clostridiaceae， and Pasteurellaceae）. Furthermore， Huangliantang improved bile acid metabolism in the serum， reducing the expression of certain bile acids ［chenodeoxycholic acid （CDCA）， tauro-alpha-muricholic acid （T-αMCA）， glycochenodeoxycholic acid （GCDCA）， glycolithocholic acid （GLCA）， glycoursodeoxycholic acid （GUDCA）， etc.）］， and these changes were significantly correlated with differential taxa of the microbiota.ConclusionHuangliantang may alleviate esophageal mucosal injury by modulating the imbalance in esophageal microbiota structure and improving abnormal bile acid metabolism， which is closely related to the regulation of the esophageal microbiota-bile acid metabolism axis.Keywords：reflux esophagitis;Huangliantang;esophageal microbiota;bile acid106|76|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Simiaosan Reduces Podocyte Apoptosis in Obese Rats with Hyperuricemia via GRP78/CHOP-endoplasmic Reticulum Stress Axis AI Introduction
Abstract：ObjectiveTo investigate the intervention effect of Simiaosan on podocyte apoptosis in obese rats with hyperuricemia and decipher the potential mechanism.MethodsForty-eight SPF-grade male SD rats were randomized into a control group， a model group， low-， medium-， and high-dose （1.09， 2.19， 4.37 g·kg-1， respectively） Simiaosan groups， and an allopurinol （0.02 g·kg-1） group. Except the control group， the other groups were fed a high-fat diet to induce an obesity model， followed by subcutaneous injection of potassium oxonate （0.5 g·kg-1） combined with gavage of adenine （0.1 g·kg-1 suspended in 0.5%CMC-Na solution） for the modeling of hyperuricemia. Each treatment group received intervention through gavage for 30 days. Renal pathological changes were observed by hematoxylin-eosin （HE） staining. The levels of serum uric acid （SUA）， serum creatinine （Scr）， urinary protein， and inflammatory factors were measured by enzyme-linked immunosorbent assay （ELISA）. The expression of molecules related to the glucose-regulated protein 78 （GRP78）/C/EBP homologous protein （CHOP） signaling pathway and apoptosis in the renal tissue was determined by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， Western blot， and immunohistochemistry （IHC）.ResultsCompared with the control group， the model group showed increases in body weight， SUA， Scr， 24-hour urinary protein （24 h UPT）， urinary albumin-to-creatinine ratio （ACR）， blood lipids ［triglycerides （TG）， total cholesterol （TC）， and low-density lipoprotein cholesterol （LDL-C）］， and serum inflammatory factors ［interleukin （IL）-1β， tumor necrosis factor （TNF）-α， and IL-6）］ （P<0.01）. Furthermore， the model group exhibited obvious pathological injury in the renal tissue， with downregulated mRNA and protein levels of the podocyte marker protein nephrin and the anti-apoptotic protein B-cell lymphoma-2 （Bcl-2） （P<0.01） and upregulated expression of GRP78， phosphorylated （p）-protein kinase R-like endoplasmic reticulum kinase （PERK）/PERK， p-eukaryotic initiation factor 2α （eIF2α）/eIF2α， activating transcription factor 4 （ATF4）， CHOP， and the pro-apoptotic protein Bcl-2-associated X protein （Bax） （P<0.01）. Compared with the model group， all Simiaosan groups and the allopurinol group showed varying degrees of improvement in the above indicators （P<0.05， P<0.01）， with the high-dose Simiaosan group showing the most significant effects.ConclusionSimiaosan can improve renal function and alleviate podocyte injury in obese rats with hyperuricemia by inhibiting the GRP78-mediated PERK/eIF2α/ATF4/CHOP signaling pathway and alleviating endoplasmic reticulum stress-induced podocyte apoptosis.Keywords：Simiaosan;obesity with hyperuricemia;glucose-regulated protein 78 （GRP78）/C/EBP homologous protein （CHOP） signaling pathway;endoplasmic reticulum stress axis;podocyte apoptosis108|77|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Danshen Zexie Decoction Ameliorates Metabolic-associated Fatty Liver Disease with Liver Fibrosis by Regulating Glycolysis and Inhibiting NETs AI Introduction
Abstract：ObjectiveTo explore the mechanism through which Danshen Zexie decoction regulates glycolysis and the formation of neutrophil extracellular traps （NETs） to treat metabolic-associated fatty liver disease （MAFLD） with liver fibrosis.MethodsSeventy-two SD rats were randomly allocated into control， model， colchicine （0.2 mg·kg-1）， and low-， medium-， and high-dose Danshen Zexie decoction （7， 14， and 28 g·kg-1， respectively） groups， with 12 rats in each group. A rat model of MAFLD with liver fibrosis was established by feeding a high-fat diet and intraperitoneally injecting 40% carbon tetrachloride （CCl4） olive oil solution. After 8 weeks， drug interventions were administered for 4 weeks. After the experiment， levels of blood lipids， liver lipids， and liver function markers， as well as serum levels of lactate， adenosine triphosphate （ATP）， inflammatory cytokines， and fibrosis indicators were measured. Hematoxylin-eosin （HE） staining， Masson staining， and oil red O staining were performed to assess the hepatic histopathology. Immunohistochemistry was employed to detect the expressions of α-smooth muscle actin （α-SMA）， neutrophil elastase （NE）， and myeloperoxidase （MPO） in the liver. The reactive oxygen species （ROS） level was measured by immunofluorescence. Western blot was performed to measure the protein levels of glucose transporter 1 （Glut1）， hexokinase 2 （HK2）， and pyruvate kinase M2 （PKM2） in the liver.ResultsCompared with the control group， the model group showed increased serum levels of total cholesterol （TC）， triglycerides （TG）， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， hydroxyproline （HYP）， hyaluronic acid （HA）， type Ⅲ procollagen （PCⅢ）， type Ⅳ collagen （ColⅣ）， laminin （LN）， tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， interleukin-8 （IL-8）， lactate， and ATP， as well as hepatic levels of TC， TG， free fatty acids （FFA）， ROS， α-SMA， NE， MPO， PKM2， HK2， and Glut1 （P<0.01）. Meanwhile， severe lipid droplet accumulation and collagen fiber deposition were observed in the liver. Compared with the model group， Danshen Zexie decoction improved the liver function and lipid metabolism， reduced hepatic steatosis and fibrosis， and downregulated the serum levels of inflammatory factors， lactate， ATP， as well as the hepatic levels of ROS， α-SMA， NE， MPO， PKM2， HK2， and Glut1 （P<0.05， P<0.01）.ConclusionDanshen Zexie decoction treats MAFLD with liver fibrosis in rats by regulating glycolysis， inhibiting the formation of NETs， and reducing inflammatory responses.Keywords：metabolic-associated fatty liver disease;liver fibrosis;Danshen Zexie decoction;glycolysis;neutrophil extracellular trap115|77|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Regulatory Effect of Danshen Zexie Decoction on Gut Microbiota-SCFAs-GLP-1 Metabolic Axis in Rat Model of Metabolic-associated Fatty Liver Disease Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the protective effect and mechanism of Danshen Zexie decoction on metabolic associated fatty liver disease （MAFLD） by regulating the gut microbiota-short-chain fatty acids （SCFAs）-glucagon-like peptide 1 （GLP-1） metabolic axis.MethodsTen SD rats were fed a standard diet as the control group， while fifty SD rats were fed a high-fat diet to build the MAFLD model. The modeled rats were assigned into the model， Yishanfu （0.144 g·kg-1）， and low-， medium-， and high-dose Danshen Zexie decoction （2.5， 5， 10 g·kg-1， respectively） groups. After 12 weeks of modeling， drugs were administered simultaneously with the modeling for 4 weeks. Serum levels of inflammatory factors were measured. Fecal gut microbiota composition was analyzed by 16S rRNA sequencing， and levels of SCFAs were quantified by gas chromatography-mass spectrometry. Western blot was performed to determine the protein levels of G protein-coupled receptors 41/43 （GPR41/43） in the colon as well as GLP-1， GLP-1 receptor （GLP-1R）， adenosine monophosphate protein kinase （AMPK）， phosphorylated （p）-AMPK， silent mating type information regulator 2 homolog 1 （SIRT1）， nuclear factor-κB （NF-κB）， and p-NF-κB in the liver.ResultsCompared with the control group， the model group showed increased serum levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-8 （IL-8）， abundance of Firmicutes and Phascolarctobacterium， Firmicutes/Bacteroidetes （F/B） ratio， and protein level of p-NF-κB （P<0.05， P<0.01）. Furthermore， the model group exhibited decreased α diversity index of the gut microbiota， abundance of Firmicutes and Lactobacillus， content of SCFAs， and protein levels of GPR41， GPR43， GLP-1， GLP-1R， p-AMPK， and SIRT1 （P<0.01）. Compared with the model group， Danshen Zexie decoction significantly decreased the contents of inflammatory factor levels in serum （P<0.01）， increased the α diversity index of the gut microbiota， the abundance of Firmicutes and Lactobacillus， the content of SCFAs， and the protein levels of GPR41， GPR43， GLP-1， GLP-1R， p-AMPK and SIRT1 （P<0.05， P<0.01）. Moreover， it decreased the abundance of Firmicutes and Phascolarctobacterium， the F/B ratio， and the protein level of p-NF-κB （P<0.05， P<0.01）.ConclusionDanshen Zexie decoction may ameliorate MAFLD by modulating the gut microbiota-SCFAs-GLP-1 metabolic axis and suppressing inflammatory response.Keywords：metabolic-associated fatty liver disease;Danshen Zexie decoction;gut microbiota;short-chain fatty acid;glucagon-like peptide-195|84|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16- Abstract：ObjectiveTo investigate the mechanism of Danshen Zexie decoction in treating metabolic-associated fatty liver disease （MAFLD） in rats via the PTEN-induced putative kinase 1 （PINK1）/E3 ubiquitin-protein ligase （Parkin） pathway-mediated mitophagy and alleviation of mitochondrial dysfunction.MethodsSD rats were randomized into control， model， Yishanfu （0.144 g·kg-1）， and low-， medium-， and high-dose Danshen Zexie decoction （2.5， 5， and 10 g·kg-1， respectively） groups. A MAFLD model was established by feeding a high-fat diet. After 12 weeks of modeling， the corresponding drugs were administered simultaneously with the modeling for 4 weeks. Levels of blood lipids， liver function markers， adenosine triphosphatase （ATP） and hepatic lipids were measured. Hematoxylin-eosin （HE） and oil red O staining were performed to assess the hepatic histopathology. Mitochondrial ultrastructure was observed via transmission electron microscopy. Western blot was performed to assess the protein levels of PINK1， Parkin， optic atrophy 1 （Opa1）， mitochondrial fission 1 （Fis1）， dynamin-related protein 1 （Drp1）， mitofusin 2 （Mfn2）， and microtubule-associated protein 1 light chain 3 （LC3） in the liver.ResultsCompared with the control group， the model group exhibited obvious elevations in serum levels of total cholesterol （TC）， triglyceride （TG）， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， as well as hepatic levels of TC， TG， free fatty acids （FFA）， and the protein levels of Drp1 and Fis1 （P<0.01）. Conversely， the hepatic protein levels of PINK1， Parkin， Mfn2， Opa1， and LC3Ⅱ were decreased in the model group （P<0.05， P<0.01）. Meanwhile， the liver in the model group presented steatosis and mitochondrial structural damage. Compared with the model group， Danshen Zexie decoction improved lipid metabolism and liver function， hepatic steatosis， and mitochondrial damage， downregulated the protein levels of Drp1 and Fis1 （P<0.05， P<0.01）， and upregulated the protein levels of Parkin， Mfn2， Opa1， and LC3Ⅱ （P<0.05， P<0.01）. Medium- and high-dose Danshen Zexie decoction upregulated the protein level of PINK1 （P<0.05， P<0.01）.ConclusionDanshen Zexie decoction may activate the PINK1/Parkin pathway to enhance mitochondrial autophagy and alleviate mitochondrial dysfunction， thus ameliorating MAFLD.Keywords：metabolic-associated fatty liver disease;Danshen Zexie decoction;PTEN-induced putative kinase 1 （PINK1）/E3 ubiquitin-protein ligase （Parkin） signaling pathway;mitophagy;mitochondrial dysfunction95|95|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16
Danshen Zexie Decoction Ameliorates Metabolic-associated Fatty Liver Disease by Increasing Nrf2/Omi/HtrA2 Pathway-mediated Autophagic Flux AI Introduction
Abstract：ObjectiveTo explore the therapeutic effect and mechanism of Danshen Zexie decoction on metabolic-associated fatty liver disease （MAFLD） by increasing autophagic flux via the nuclear factor erythroid 2-related factor 2 （Nrf2）/high temperature requirement factor A2/Omi （Omi/HtrA2） pathway.MethodsTen SD rats were fed a standard diet as the control group， while 50 SD rats were fed a high-fat diet to build the MAFLD model. The modeled rats were randomly assigned into model， Yishanfu （0.144 g·kg-1）， and low-， medium-， and high-dose Danshen Zexie decoction （2.5， 5， and 10 g·kg-1， respectively） groups. After 12 weeks of modeling， drugs were administered simultaneously for 4 weeks. Levels or activities of superoxide dismutase （SOD）， glutathione peroxidase （GSH-Px） and malondialdehyde （MDA） were measured. The hepatic reactive oxygen species （ROS） level was detected by immunofluorescence. Western blot was performed to assess the protein levels of Nrf2， Omi/HtrA2， hematopoietic cell-specific protein 1-associated protein X-1 （Hax-1）， optic atrophy protein 1 （Opa1）， mitochondrial dynamin-related protein 1 （Drp1）， autophagy key molecule mammalian ortholog of yeast Atg6 （Beclin1）， selective autophagy junction protein 62 （p62）， and microtubule-associated protein 1 light chain 3 （LC3） in the liver.ResultsCompared with the control group， the model group exhibited obviously elevation in serum level of MDA， hepatic level of ROS， and protein levels of Hax-1， Drp1 and p62 （P<0.01）. Conversely， the serum activities of SOD and GSH-Px， as well as hepatic protein levels of Nrf2， Omi/HtrA2， Opa1， Beclin1 and LCⅡ were decreased in the model group （P<0.01）. Danshen Zexie decoction alleviated oxidative stress， lowered the protein levels of Hax-1， Drp1， and p62 （P<0.05， P<0.01）， and increased the protein levels of Nrf2， Omi/HtrA2， Opa1， Beclin1 and LCⅡ （P<0.05， P<0.01）.ConclusionDanshen Zexie decoction may treat MAFLD by increasing autophagic flux and alleviating mitochondrial dysfunction through regulating the Nrf2/Omi/HtrA2 pathway.Keywords：metabolic-associated fatty liver disease;Danshen Zexie decoction;nuclear factor erythroid 2-related factor 2 （Nrf2）;high temperature requirement factor A2/Omi （Omi/HtrA2）;autophagic flux75|79|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Xiaoyaosan Combined with Fuzi Lizhongwan Reduces High-fat Diet-induced Depressive-like Behavior in Rats with Spleen Deficiency by Regulating Mitochondrial Energy Metabolism and Glycolysis Reprogramming Enhanced Publication AI Introduction
Abstract：ObjectiveTo explore the effect of Fuzi Lizhongwan combined with Xiaoyaosan on the high-fat diet-induced depressive-like behavior in rats with spleen deficiency by focusing on mitochondrial energy metabolism and glycolysis reprogramming.MethodsA high-fat diet was used for the modeling of depressive-like behavior in a rat model of spleen deficiency. Rats were assigned into control， spleen deficiency， high-fat diet， spleen deficiency + high-fat diet， Fuzi Lizhongwan （1.5 g·kg-1·d-1）， Xiaoyaosan （1.01 g·kg-1·d-1）， and combined treatment （Fuzi Lizhongwan + Xiaoyaosan， 2.51 g·kg-1·d-1） groups. Depression-like behavior was assessed by sucrose preference， open field， and forced swimming tests. Hematoxylin-eosin （HE） staining and Nissl staining were conducted to observe pathological changes in the hippocampus， and oil red O staining to assess lipid deposition in the liver. Enzyme-linked immunosorbent assay （ELISA） was performed to measure 5-hydroxytrypatamine （5-HT）， dopamine （DA）， lipid， and inflammatory factor levels. Non-targeted proteomics and metabolomics were employed to analyze energy metabolism and glycolysis pathways. Adenosine triphosphate （ATP） content and mitochondrial function were measured. Mitochondrial function， AMP-activated protein kinase （AMPK） pathway， and glycolysis-related indicators were assessed by Real-time PCR and Western blot. Furthermore， lactate and pyruvate levels were measured.ResultsCompared with the control group， the spleen deficiency + high-fat diet group showed reduced spontaneous behavior and sucrose consumption and prolonged immobile time in the forced swimming test （P<0.05）， hippocampal damage， hippocampal damage， reduced Nissl bodies， and increased hepatic lipid deposition. Furthermore， this group exhibited declined levels of 5-HT， DA， and ATP， weakened function of the mitochondrial respiratory chain， elevated levels of lipids， inflammatory factors， and glycolysis-related indicators， along with abnormally elevated phosphorylation levels of the AMPK/ACC pathway （P<0.05）. The combined treatment significantly alleviated these abnormalities， with better effects than Fuzi Lizhongwan or Xiaoyaosan alone.ConclusionFuzi Lizhongwan combined with Xiaoyaosan synergistically regulates mitochondrial energy metabolism and glycolysis reprogramming to restore energy homeostasis and reduce the high-fat diet-induced depressive-like behavior in rats with spleen deficiency.Keywords：Xiaoyaosan;Fuzi Lizhongwan;depression;mitochondrial energy metabolism;glycolysis reprogramming74|78|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Xuming Tongmai Decoction Regulates Autophagy and Apoptosis in Brain Tissue of Stroke Rats Through mTOR/HIF-1α/VEGF Signaling Pathway AI Introduction
Abstract：ObjectiveTo investigate the effects of Xuming Tongmai decoction on autophagy and apoptosis in the brain tissue of stroke rats based on the mammalian target of rapamycin （mTOR）/hypoxia-inducible factor-1α （HIF-1α）/vascular endothelial growth factor （VEGF） signaling pathway.MethodsThe permanent middle cerebral artery occlusion model was established in rats through the suture-occlusion method. Rats were randomly allocated into the following groups （n=10 per group）： sham， model， low-， medium-， and high-dose Xuming Tongmai decoction （6.45， 12.90， 25.80 g·kg-1， respectively， gavage）， nimodipine （0.012 g·kg-1， gavage）， and Xuming Tongmai decoction （25.80 g·kg-1， gavage） + rapamycin （20 mg·kg-1， intraperitoneal injection）. All treatments lasted for 7 consecutive days. Neurological function was assessed based on the modified neurological severity score （mNSS） and the Zea-Longa score. Pathological damage in the rat brain tissue was examined by hematoxylin-eosin （HE） and Nissl staining. The expression of proteins related to the mTOR/HIF-1α/VEGF signaling pathway in the brain tissue was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and immunohistochemistry （IHC）. The expression of apoptosis-related proteins was determined by Western blot. The expression of microglial polarization markers， inflammatory factors， and angiogenesis indicators in the brain tissue was measured by enzyme-linked immunosorbent assay （ELISA）， immunofluorescence， and Real-time PCR.ResultsCompared with the sham group， the Model group showed increased mNSS and Zea-Longa scores， loose arrangement of hippocampal neurons， karyopyknosis， vacuolation， significant inflammatory cell infiltration， and reduced Nissl body count in the brain tissue. In addition， the model group exhibited decreased expression of mTOR， HIF-1α， and VEGF at mRNA and protein levels， increased expression of cleaved cysteinyl aspartate-specific proteinase-3 （Caspase-3） and Bcl-2-associated X protein （Bax）， decreased expression of B-cell lymphoma-2 （Bcl-2）， elevated levels of interleukin （IL）-1β and IL-6， declined levels of IL-4 and IL-10， reduced protein level of arginase-1 （Arg1）， increased protein level of ionized calcium-binding adapter molecule 1 （Iba1）， and down-regulated mRNA levels of von Willebrand factor （vWF）， stromal cell-derived factor （SDF）-1α， and C-X-C chemokine receptor type 4 （CXCR4） （P<0.05， P<0.01）. Compared with the model group， both the high-dose Xuming Tongmai decoction group and the nimodipine group restored the above indicators （P<0.01）. Compared with the high-dose Xuming Tongmai decoction group， the Xuming Tongmai decoction + rapamycin group aggravated the above indicators （P<0.05， P<0.01）.ConclusionXiuming Tongmai decoction can regulate the mTOR/HIF-1α/VEGF signaling pathway to promote angiogenesis and inhibit neuronal autophagy and apoptosis， thereby improving the neurological function of stroke rats and exerting neuroprotective effect.Keywords：Xuming Tongmai decoction;stroke;autophagy;apoptosis;angiogenesis;neurological function;mammalian target of rapamycin （mTOR）/hypoxia-inducible factor 1-α （HIF-1α）/vascular endothelial growth factor （VEGF） signaling pathway92|88|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Mechanism of Huoxin Pills in Stabilizing Atherosclerotic Vulnerable Plaque Based on Network Pharmacology and Metabolomics Enhanced Publication AI Introduction
Abstract：ObjectiveBased on network pharmacology， non-targeted metabolomics， and animal models， this study aims to investigate the stabilizing effect of Huoxin pills on atherosclerotic（AS） vulnerable plaques and the molecular mechanism of action.MethodsA total of 40 SPF male apolipoprotein E knockout （ApoE-/-） mice were fed a high-fat diet for 12 weeks to establish AS models. They were randomly divided into a model group， an atorvastatin group （2.5 mg·kg-1·d-1）， a low-dose Huoxin pill group （18.2 mg·kg-1·d-1）， and a high-dose Huoxin pill group （36.4 mg·kg-1·d-1）， with 10 mice in each group. Additionally， 10 C57BL/6J mice were designated as the control group. The model group and control group were administered equal volumes of saline via gavage daily， while each treatment group received the corresponding drug dose via gavage. After 8 weeks of intervention， an ultrasound was used to measure the difference between diastolic diameter and systolic diameter （Dd-Ds） of the aorta and carotid arteries， as well as pulse wave velocity （PWV）. Biochemical assays were performed to measure total cholesterol （TC）， triglycerides （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） levels in serum. Enzyme-linked immunosorbent assay （ELISA） was used to determine interleukin （IL）-6， IL-1β， and tumor necrosis factor-α （TNF-α） levels in the serum of mice. The aortic root plaque area， lipid content， collagen， macrophage （CD68）， and α-smooth muscle actin （α-SMA） expression were assessed by hematoxylin and eosin （HE）， oil red O， Masson， and immunohistochemical staining. The plaque vulnerability index （VI） was calculated. Additionally， oil red O staining of the liver was performed to observe lipid deposition and measure the hepatic TC contents. Predictive analysis of core targets of drugs and diseases was conducted using network pharmacology， and non-targeted metabolomics techniques were employed to identify key differentially expressed metabolites and their associated pathways. Western blot and real-time quantitative PCR （Real-time PCR） assays were employed to detect the protein and mRNA expressions of peroxisome proliferator-activated receptor γ （PPARγ）， liver X receptor α （LXRα）， phosphorylated nuclear factor-κB p65 （p-NF-κB p65）， nuclear factor-κB p65 （NF-κB p65）， ATP-binding cassette transporter A1 （ABCA1）， ATP-binding cassette transporter G1 （ABCG1）， and IL-6 in the liver tissue of mice.ResultsIn vivo animal experiment results show that Huoxin pills reduce PWV values in the aortic arch of ApoE-/- mice （P<0.05） and increase the Dd-Ds value in the aorta （P<0.05）， effectively improving vascular elasticity and reducing arterial stiffness. Huoxin pills reduced the proportion of lipid plaque area in the aortic arch （P<0.01）， decreased lipid deposition in the liver （P<0.01）， reduced lipid content and macrophage infiltration in plaques （P<0.05）， increased collagen deposition and smooth muscle cell content （P<0.05）， lowered plaque VI （P<0.01）， and regulated blood lipid levels （P<0.05）. Integrated metabolomics and network pharmacology analyses reveal that Huoxin pills ultimately exert a pharmacological effect on stabilizing AS vulnerable plaques by activating the PPARγ nuclear receptor， upregulating the expression of the PPARγ/LXRα/ABCA1/ABCG1 pathway， thereby facilitating cholesterol efflux from macrophages and inhibiting NF-κB/IL-6 inflammatory responses. Western blot and Real-time PCR results show that Huoxin pills can upregulate the protein and mRNA expressions of PPARγ， LXRα， ABCA1， and ABCG1 in the liver tissue of ApoE-/- mice （P<0.05） and downregulate the expression levels of NF-κB and IL-6 （P<0.05）.ConclusionHuoxin pills may enhance the stability of AS vulnerable plaques by regulating the PPARγ/LXRα/ABCA1/ABCG1 pathway and suppressing inflammation， thereby reducing lipid deposition and macrophage infiltration within the plaques.Keywords：atherosclerosis;Huoxin pills;vulnerable plaque;metabolomics;network pharmacology;peroxisome proliferator-activated receptor γ（PPARγ）/liver X receptor α（LXRα）/ATP-binding cassette transporter A1 （ABCA1）/ATP-binding cassette transporter G1（ABCG1） signaling pathway140|75|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Effect of Didang Tang on Microglial Pyroptosis in Rats with Cerebral Infarction of Stasis-heat Syndrome Based on JAK2/STAT3 Signaling Pathway AI Introduction
Abstract：ObjectiveThis paper aims to investigate the effects of Didang Tang on microglial pyroptosis and cerebral infarction of stasis-heat syndrome through regulation of the Janus kinase 2/signal transducer and activator of transcription 3（JAK2/STAT3） signaling pathway.MethodsSixty rats were randomly divided into a sham group， a model group， low-， medium-， and high-dose Didang Tang groups（0.95， 1.89， 3.78 g·kg-1）， and an edaravone group（3.20 mg·kg-1）， with ten rats per group. Except for the sham group， a cerebral infarction of stasis-heat syndrome model was established by middle cerebral artery occlusion/reperfusion（MCAO/R） combined with intraperitoneal injection of carrageenan（50 mg·kg-1） for three days and subcutaneous injection of dry yeast（10 mL·kg-1） for one day. Twenty-four hours later， the rats in the Didang Tang groups received intragastric administration， and those in the edaravone group received intraperitoneal injection for seven days. Neurological deficits were evaluated by the modified neurological severity score（mNSS）. Cerebral infarct volume was assessed by 2，3，5-triphenyltetrazolium chloride（TTC） staining. The concentrations of whole blood and plasma were measured by hemorheology. Additionally， 36 rats were randomly divided into a sham group， a model group， a high-dose Didang Tang group， and an AG490 group（5 mg·kg-1）， with nine rats per group. Modeling and drug administration were performed as above. The rats in the AG490 group received AG490 via intraperitoneal injection for seven consecutive days. Hematoxylin-eosin（HE） staining and Nissl staining were used to observe the pathological morphology of brain tissues. Western blot was used to detect expression levels of the proteins related to the JAK2/STAT3 pathway and pyroptosis. Real-time polymerase chain reaction（Real-time PCR） was used to detect pyroptosis-related mRNA levels. An enzyme-linked immunosorbent assay（ELISA） was used to measure the levels of interleukin（IL）-1β， IL-18， IL-6， and tumor necrosis factor-α（TNF-α） in serum. Immunofluorescence staining（IF） was used to detect ionized calcium-binding adapter molecule-1/gasdermin D（Iba-1/GSDMD） co-expression. A transmission electron microscope was used to observe membrane pore formation in microglia.ResultsCompared with those in the sham group， the rats in the model group show significantly increased neurological deficit scores， cerebral infarct volume， the whole blood viscosity at high， medium and low shear rates， plasma viscosity， pyroptosis-related protein and mRNA expressions， phosphorylation levels of the JAK2/STAT3 pathway， the levels of IL-1β， IL-18， IL-6， and TNF-α， Iba-1 and GSDMD fluorescence areas， pyroptosis rate， and microglial membrane pore number（P<0.01）， accompanied by significantly deteriorated pathological structure and neuronal survival of brain tissue on the ischemic side. Compared with those in the model group， the rats in the high-dose Didang Tang group exhibit significantly reduced indicators（P<0.05， P<0.01）， improved pathological injury and neuronal survival in brain tissues， and better effects than those in the medium- and low-dose Didang Tang groups.ConclusionThe JAK2/STAT3 signaling pathway is involved in regulating NOD-like receptor protein 3（NLRP3） inflammasome-mediated microglial pyroptosis. Didang Tang may alleviate microglial pyroptosis and exert neuroprotective effects on cerebral infarction of stasis-heat syndrome by inhibiting the activation of this pathway.Keywords：cerebral infarction;stasis-heat syndrome;Janus kinase 2/signal transducer and activator of transcription 3（JAK2/STAT3） signaling pathway;microglia;pyroptosis;Didang Tang96|87|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Quansanqi Tablets Ameliorate Myocardial Injury via MAPK and NF-κB Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the protective effect of Quansanqi tablets （PSQ） against acute myocardial ischemia （MI） and explore the mechanism of PSQ in ameliorating myocardial injury based on the main effector cells.MethodsIn the animal experiment， KM mice were randomized into the normal， model， propranolol， and PSQ （0.3， 0.6， 1.2 g·kg-1） groups. A mouse model of acute MI was established by intraperitoneal injection of isoproterenol hydrochloride （ISO）. Electrocardiogram （ECG） was recorded. The levels of lactate dehydrogenase （LDH） and malondialdehyde （MDA） in the serum and superoxide dismutase （SOD） in the myocardial tissue were measured by colorimetric methods. The serum level of creatine kinase isoenzyme （CK-MB） was determined by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） staining was used to observe pathological changes in the myocardial tissue. In the cell experiment， lipopolysaccharide （LPS） was used to induce injuries in rat myocardial cells （H9C2 cells） and mouse macrophages （RAW264.7 cells）. H9C2 cells were allocated into normal， model， and PSQ （12.5， 25， 50 mg·L-1） groups， and RAW264.7 cells were assigned into normal， model， and PSQ （25， 50， 100 mg·L-1） groups. Cell viability was measured by the cell counting kit-8 （CCK-8） assay. Cellular MDA and LDH levels were measured by colorimetric methods. The levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）. Apoptosis， cell cycle， reactive oxygen species （ROS）， and nitric oxide （NO） levels were measured by flow cytometry. The expression and phosphorylation levels of c-Jun N-terminal kinase （JNK）， p38 mitogen-activated protein kinase （MAPK）， extracellular signal-regulated kinase （ERK）， and nuclear factor-kappa B （NF-κB） p65 were determined by Western blot.ResultsThe animal experiment showed that compared with the normal group， the model group exhibited ST segment elevation and T wave inversion on ECG， raised serum LDH， CK-MB， and MDA levels （P<0.01）， and hemorrhage， inflammatory infiltration， edema， and myocardial cell deformation in the myocardial tissue. Compared with the model group， PSQ at different doses alleviated ST segment elevation and T wave inversion on ECG， reduced serum LDH and CK-MB levels （P<0.05， P<0.01）， increased SOD content in the myocardial tissue （P<0.05）， and ameliorated pathological changes in the myocardial tissue. The cell experiment showed that compared with the normal group， the model group showcased decreased H9C2 cell viability （P<0.01）， increased G1 phase cell proportion， decreased S phase proportion （P<0.05）， and elevated MDA， ROS， NO， and LDH levels （P<0.01）. The RAW264.7 cells showed increased apoptosis rate （P<0.01）， elevated IL-1β， IL-6， and TNF-α levels （P<0.01）， and raised phosphorylation levels of JNK， p38 MAPK， ERK， and NF-κB p65 in both cell lines （P<0.01）. Compared with the model group， PSQ at various concentrations increased H9C2 cell viability （P<0.01）， improved cell cycle status （P<0.05， P<0.01）， reduced MDA， ROS， NO， and LDH levels （P<0.05， P<0.01）， decreased the apoptosis rate and inflammatory factor levels in RAW264.7 cells （P<0.01）， and lowered the phosphorylation levels of JNK， p38 MAPK， ERK， and NF-κB p65 in both cell lines （P<0.05， P<0.01）.ConclusionPSQ can ameliorate ISO-induced myocardial injury in mice and significantly enhance the viability and anti-inflammatory and antioxidant capacity of myocardial cells and macrophages by regulating the MAPK and NF-κB signaling pathway.Keywords：Quansanqi tablets;macrophages;cardiomyocytes;myocardial injury;mitogen-activated protein kinase （MAPK）;nuclear factor-kappa B （NF-κB）90|475|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Notoginseng Total Saponins Ameliorate Doxorubicin-induced Cardiotoxicity by Inhibiting Ferroptosis via Activation of Nrf2 Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the protective effect of Notoginseng total saponins （NTS） against doxorubicin （DOX）-induced cardiotoxicity （DIC） and to explore the specific mechanism by which NTS inhibits ferroptosis via the nuclear facor erythroid 2-related factor 2 （Nrf2） signaling pathway.MethodsC57BL/6 mice were assigned into control， DOX （6 mg·kg-1）， low-dose （3 g·kg-1） NTS + DOX （Low NTS+DOX）， high-dose （6 g·kg-1） NTS + DOX （High NTS+DOX）， and dexrazoxane （30 mg·kg-1） + DOX （DEX+DOX） groups （n=10 per group）. On days 6 and 9， other groups except the control group received intravenous injections of DOX. The control group was injected with an equal volume of normal saline （0.9%NaCl） at the same time points. Thirty minutes before each DOX injection， the DEX+DOX group was intravenously administered DEX. The NTS-treated groups received daily oral gavage of NTS dissolved in ultrapure water for 12 days， starting 5 days before DOX administration. The control and DOX groups were administered an equal volume of distilled water by gavage during the same period. Cardiac function was assessed by echocardiography. The myocardial injury was evaluated by hematoxylin-eosin （HE） staining and serum cardiac injury markers. The iron（Ⅱ） ion （Fe2+） level and lipid peroxidation were measured via commercial kits. Apoptosis was observed by terminal deoxygenucleotidyl transferase dUTP nick-end labeling （TUNEL） staining. Nrf2 nuclear translocation and the expression of downstream proteins including nuclear receptor coactivator 4 （NCOA4）， ferroportin （FPN）， glutathione peroxidase 4 （GPX4） and transferrin receptor 1 （TfR1）were examined by immunofluorescence and Western blot.ResultsCompared with the control group， the DOX group showed decreased left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01）， elevated levels of creatine kinase-MB （CK-MB） and lactate dehydrogenase （LDH） （P<0.01）， increased Fe2+ and malondialdehyde （MDA） （P<0.01）， and reduced glutathione （GSH） （P<0.01）. Western blot analysis revealed downregulated expression of Nrf2， FPN， GPX4， and TfR1 （P<0.05， P<0.01）， and upregulated expression of NCOA4 （P<0.01）. Compared with the DOX group， NTS improved LVFS and LVEF （P<0.05， P<0.01）， decreased CK-MB and LDH levels （P<0.01）， lowered Fe2+ and MDA levels （P<0.01）， and increased the GSH level （P<0.05）. At the protein level， NTS enhanced the expression of Nrf2 and GPX4 （P<0.05， P<0.01） and showed a regulatory trend on the expression of FPN， TfR1， and NCOA4， although these changes were not statistically significant.ConclusionNTS can alleviate DOX-induced cardiotoxicity by inhibiting ferroptosis through activation of the Nrf2 signaling pathway.Keywords：doxorubicin-induced cardiotoxicity;ferroptosis;Notoginseng total saponins;nuclear facor erythroid 2-related factor 2 （Nrf2）80|107|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Action Mechanism of Betulinic Acid in Inhibiting Ferroptosis and Improving Non-alcoholic Fatty Liver Disease Based on Bioinformatics and Experimental Validation Enhanced Publication AI Introduction
Abstract：ObjectiveThis paper aims to investigate the action mechanism of betulinic acid （BA） in inhibiting ferroptosis and improving non-alcoholic fatty liver disease （NAFLD） through bioinformatics analysis and experimental validation， providing references for both basic research and clinical applications of NAFLD.MethodsBased on bioinformatics analysis， the NAFLD-related microarray datasets， GSE89632 and GSE63067， were downloaded from the gene expression omnibus （GEO） database. Ferroptosis-related genes were downloaded from the ferroptosis database， and differentially expressed genes （DEGs） related to NAFLD ferroptosis were screened to construct enrichment analyses of protein-protein interaction （PPI） networks， gene ontology （GO）， and Kyoto encyclopedia of genes and genomes （KEGG）. Different algorithms were used to mine key DEGs， which were further analyzed for correlation， immune infiltration， and immune cell differences of key DGEs. Least absolute shrinkage and selection operator （LASSO） regression analysis was conducted to identify disease feature genes from the key DEGs. The intersection of key genes from various algorithms of Cytoscape and the disease feature genes identified through LASSO regression was used to select core genes. The survival curve， namely receiver operating characteristic （ROC） curve， was performed to validate these core genes. Potential new targets for NAFLD were analyzed and predicted， and molecular docking was used to verify the core targets and active components of traditional Chinese medicine. Animal experiment was conducted. Fifty C57BL/6J mice were randomly divided into the normal group， model group， low-dose/high-dose BA groups， and silymarin group. The model was established by feeding a high-fat and high-cholesterol diet combined with 2.5% dextran sulfate sodium （DSS） in drinking water， followed by continuous gavage for 24 days in the drug groups. Body weight and liver index of mice were measured at sampling， and hematoxylin and eosin （HE） staining was used to assess hepatic lipid droplet deposition. Western blot and real-time polymerase chain reaction （Real-time PCR） were performed to detect the expression levels of glutathione peroxidase 7 （GPX7）， lactotransferrin （LTF）， S100 calcium binding protein A8 （S100A8）， ferroptosis markers GPX4， and acyl-CoA synthetase long-chain family member 4 （ACSL4） at the protein and mRNA levels.ResultsData analysis identified 10 key genes in the ferroptosis process of NAFLD， including SUMO-specific peptidase 1 （SENP1）， aldo-keto reductase family 1 member C3 （AKR1C3）， and others. Least absolute shrinkage and selection operator- receiver operating characteristic （LASSO-ROC） analysis confirmed that GPX7， LTF， and S100A8 were core genes ［area under the curve（AUC）=0.771-0.821］. KEGG enrichment analysis revealed that these differentially expressed genes were involved in ferroptosis， advanced glycation end-products/receptor （AGE/RAGE）， and other pathways. Correlation analysis of key genes in ferroptosis process of NAFLD showed significant positive correlations between SENP1 and AKR1C3 as well as other genes （P<0.01）， and significant negative correlations between dipeptidyl peptidase 4 （DPP4） and GPX7 as well as other genes （P<0.01）. Immune infiltration analysis showed that myeloid-derived suppressor cells （MDSCs）， activated dendritic cells， and other immune cells were the primary immune cells infiltrating in NAFLD and involved in the ferroptosis process. Differential correlation analysis of immune cell revealed a significant negative correlation between GPX7 and follicular helper T cells as well as others （P<0.01）， while S100A8 showed a significant positive correlation with MDSCs （P<0.01）. In the animal experiments， NAFLD mice with BA intervention showed significantly reduced liver index and lipid droplet deposition. Compared to the normal group， the model group exhibited significantly increased proteins/mRNA levels of S100A8 and ACSL4 （P<0.01） and significantly decreased levels of LTF， GPX7， and GPX4 （P<0.01）. In comparison with the model group， both the silymarin and BA groups partially reversed these trends in a dose-dependent manner.ConclusionBA may inhibit the ferroptosis process and alleviate liver inflammation and lipid deposition by regulating GPX7， LTF， and S100A8. The mechanism is related to the restoration of GPX4 activity and downregulation of ACSL4 expression.Keywords：bioinformatics;betulinic acid;molecular docking;non-alcoholic fatty liver disease;ferroptosis97|113|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Mechanisms of Celastrus orbiculatus Ethylacetate Extract in Regulating M2 Macrophage Polarization to Inhibit Gastric Cancer Proliferation and Migration Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the effects of Celastrus orbiculatus ethylacetate extract （COE） on macrophage polarization and the underlying mechanisms in inhibiting the proliferation and migration of gastric cancer cells.MethodsTHP-1 cells were stimulated with phorbol 12-myristate 13-acetate （PMA）， interleukin-4 （IL-4）， and interleukin-13 （IL-13） to establish an M2 macrophage polarization model. The cells were divided into three groups： M0 group （treated with PMA at 100 μg·L-1）， M2 group （treated with PMA at 100 μg·L-1 + IL-4 and IL-13 at 20 μg·L-1 each）， and M2 + COE group （treated with PMA at 100 μg·L-1 + IL-4 and IL-13 at 20 μg·L-1 each， and COE at 10 mg·L-1）. Cell viability was assessed using the cell counting kit-8（CCK-8） assay， and cell proliferation was evaluated by the EdU assay. The mRNA expression levels of macrophage polarization markers， including interleukin-10 （IL-10）， cluster of differentiation 206 （CD206）， tumor necrosis factor-α （TNF-α）， and cluster of differentiation 86 （CD86）， were determined by Real-time PCR. The levels of IL-10 and TNF-α in macrophage supernatants were measured by ELISA. Western blot were performed to evaluate the expression of migration‑related proteins in gastric cancer cells treated with conditioned medium （CM） from COE‑treated macrophages.ResultsCCK-8 and EdU assays showed that， compared with the M2-CM group， the M2 + COE-CM group significantly inhibited the proliferation of gastric cancer cells （P<0.05， P<0.01）. Compared with the M0 group， the mRNA expression levels of IL-10 and CD206 in macrophages were significantly increased in the M2 group （P<0.01）. Compared with the M2 group， the M2 + COE group showed significantly decreased mRNA expression of IL-10 and CD206 （P<0.01）， while the mRNA expression of TNF-α and CD86 was significantly increased （P<0.01）. In addition， the level of IL-10 in the supernatant was decreased， whereas the level of TNF-α was significantly increased （P<0.05， P<0.01）. Western blot analysis demonstrated that， compared with the M2-CM group， the protein expression levels of Vimentin， MMP-2， MMP-9， Snail， and Slug in AGS， HGC-27， and MKN28 cells were significantly reduced in the M2 + COE-CM group （P<0.05， P<0.01）.ConclusionCOE can inhibit the proliferation and migration of gastric cancer cells by regulating macrophage polarization. The underlying mechanisms may be closely associated with the regulation of the epithelial-mesenchymal transition （EMT） process via the TLR4/NF-κB signaling pathway.Keywords：Celastrus orbiculatus ethylacetate extract;gastric cancer;proliferation;migration;macrophage polarization176|97|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Protective Effect of Kummerowia striata Extract Against Carbon Tetrachloride-induced Acute Liver Injury in Mice Based on Gut Microbiota-Nrf2/NF-κB/MAPK Axis Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the effects of Kummerowia striata extract on inflammatory response， oxidative stress， and gut microbiota in mice with acute liver injury （ALI） induced by carbon tetrachloride （CCl4）.MethodsSixty male Kunming mice were randomly divided into six groups （n=10 per group）： Blank control group， model group， bifendate group （150 mg·kg-1）， and high-， medium-， and low-dose groups of K. striata extract （600， 400， and 200 mg·kg-1， respectively）. All treatments were administered continuously by gavage for 14 days. An ALI model was established by intraperitoneal injection of 0.2%CCl4 in olive oil solution 2 h after the last administration. Serum， liver tissues， and cecal contents were collected 16 h later. Serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST） activity， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6） were measured. The activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px）， as well as the content of malondialdehyde （MDA） were determined in liver tissues. Hepatic histopathological changes were observed by hematoxylin-eosin （HE） staining. Western blot was used to detect the expression levels of phosphorylated nuclear factor-κB p65 （p-NF-κB p65）， phosphorylated extracellular signal-regulated kinase （p-ERK）， phosphorylated c-Jun N-terminal kinase （p-JNK）， phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK）， nuclear factor erythroid 2-related factor 2 （Nrf2）， heme oxygenase-1 （HO-1）， and Kelch-like ECH-associated protein1 （Keap1） in liver tissues. 16S rDNA high-throughput sequencing technology was used to detect changes in gut microbiota in cecum contents.ResultsMedium and low-dose groups of K. striata extract significantly reduced serum ALT and AST activities and lowered TNF-α and IL-6 levels in mice with ALI（P<0.05，P<0.01）. The extract also increased SOD and GSH-Px activities， decreased MDA content in liver tissues， and ameliorated histopathological damage（P<0.05，P<0.01）. Furthermore， the extract upregulated Nrf2 and HO-1 expression，downregulated the protein expression of Keap1， p-NF-κB p65， p-p38 MAPK， p-ERK， and p-JNK （P<0.05，P<0.01）， and alleviated gut microbiota dysbiosis.ConclusionK. striata extract exerted a significant protective effect against CCl4-induced acute liver injury in mice. The mechanism may be associated with the activation of Nrf2/HO-1 signaling pathway to alleviate oxidative damage， regulation of nuclear factor-κB （NF-κB）/mitogen-activated protein kinase （MAPK） signaling pathway to suppress inflammatory response， and improvement of gut microbiota dysbiosis via the gut-iver axis.Keywords：Kummerowia striata extract;liver injury;nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway;nuclear factor-κB （NF-κB）/mitogen-activated protein kinase （MAPK） signaling pathway;gut microbiota87|442|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Clinical Efficacy of Yiqi Jianyun Prescription in Treating Obesity Associated with Qi-deficiency Constitution Enhanced Publication AI Introduction
Abstract：ObjectiveTo explore the clinical efficacy of Yiqi Jianyun prescription （YQJYP） in treating obesity associated with Qi-deficiency constitution.MethodsA 12-week randomized controlled clinical trial was conducted with 90 patients diagnosed with obesity and Qi-deficiency constitution. The control group received no intervention， while the observation group was treated with YQJYP for 12 weeks. Both groups maintained their usual lifestyle habits. After 12 weeks， obesity-related parameters， Qi-deficiency constitution scores， and safety outcomes were evaluated. Additionally， fecal samples from the observation group were collected before and after treatment for gut microbiota sequencing and fatty acid profiling.ResultsA total of 35 participants in the control group and 39 in the observation group completed the trial， with an overall completion rate of 82.22%. Compared with baseline， the observation group showed reductions in body weight， body mass index （BMI）， waist circumference， waist-to-hip ratio （WHR）， total cholesterol （TC）， triglycerides （TG）， low-density lipoprotein cholesterol （LDL-C）， fasting blood glucose （FBG）， glycated hemoglobin （HbA1c）， and Qi-deficiency constitution score （P<0.01）， while remaining unchanged high-density lipoprotein cholesterol （HDL-C）. The control group showed increases in TC and TG （P<0.05， P<0.01） and no significant changes in other indicators. After treatment， compared with the control group， the observation group exhibited decreases in body weight， BMI， waist circumference， WHR， TC， TG， LDL-C， FBG， HbA1c， and Qi-deficiency constitution score （P<0.05， P<0.01）， with no significant difference in HDL-C. No significant adverse events were observed in either group during the 12 weeks. Gut microbiota analysis in the observation group revealed that YQJYP increased the Sobs， Ace， Chao， and Shannon indices （P<0.01）， reduced the dysbiosis index， and elevated the relative abundance of Actinomycetota， Blautia， and Bifidobacterium， while decreasing the relative abundance of Streptococcus and Collinsella （P<0.05， P<0.01）. Fatty acid profiling indicated that treatment increased the content of short-chain fatty acids and reduced the content of medium- and long-chain fatty acids （P<0.05， P<0.01）.ConclusionYQJYP can safely and effectively reduce body weight， BMI， and WHR and improve glucose and lipid metabolism in patients with obesity and Qi-deficiency constitution by regulating the gut microbiota and fatty acid metabolism.Keywords：Yiqi Jianyun prescription;Qi-deficiency constitution;obesity;clinical efficacy81|68|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16A Randomized Controlled Trial of Wenyang Jiedu Granules in Treatment of Severe COVID-19 Enhanced Publication AI Introduction
Abstract：ObjectiveTo evaluate the efficacy and safety of Wenyang Jiedu granules combined with conventional Western medicine in the treatment of severe coronavirus disease 2019 （COVID-19）.MethodsA multicenter， open-label， randomized controlled clinical trial was conducted. Eligible patients were randomly divided into the observation group and the control group at a 1∶1 ratio. The control group received conventional Western medicine treatment in accordance with the Diagnosis and Treatment Protocol for COVID-19 （Trial Version 10）. On the basis of conventional Western medicine treatment， the observation group was additionally given Wenyang Jiedu granules， 2 sachets （30 g） each time， three times a day， with a treatment course of 14 days. The primary outcome was the proportion of clinical progression on day 14， and the secondary outcomes included mortality， the proportion of clinical improvement and the incidence of composite clinical events at day 7， 14 and 28 as well. The prognostic differences were compared between the two groups.ResultsA total of 185 participants were enrolled， including 91 cases in the observation group and 94 cases in the control group. The baseline characteristics were balanced and comparable between the two groups. After excluding 2 incorrectly enrolled cases， 183 patients were included in the modified intention-to-treat （mITT） set； after excluding cases of dropout and protocol violation， 151 patients were included in the per-protocol set （PPS）. The results of both analysis sets showed that the proportion of clinical progression on day 14 in the observation group was significantly lower than that in the control group （mITT： 7.9% vs 18.1%， P=0.041； PPS 4.0% vs 17.1%， P=0.015）. Subgroup analysis indicated that the observation group achieved more obvious efficacy（P<0.05） in patients aged over 60 years ［relative risk （RR）=0.367， 95% confidence interval （95%CI）： 0.143-0.941］， patients with diabetes （RR=0.183， 95%CI： 0.036-0.930）， and patients without chronic respiratory diseases （RR=0.357， 95%CI 0.130-0.981）. Compared with the control group， the observation group had significantly lower incidence of composite clinical events at day 7 （22.5% vs 39.4%， P=0.014） and day 14 （39.3% vs 54.3%， P=0.043）. The mortality at day 7， 14 and 28， the proportion of clinical progression at day 7 and 28， the rate of invasive mechanical ventilation， and the rate of non-invasive mechanical ventilation/high-flow oxygen therapy showed a downward trend， while the proportion of clinical improvement at day 7， 14 and 28 showed an upward trend， without statistically significant differences. There was no significant difference in the incidence of adverse events between the two groups.ConclusionWenyang Jiedu granules can reduce the risk of disease progression on day 14 in patients with severe COVID-19， with more prominent advantages in patients aged over 60 years， patients complicated with diabetes， and patients without chronic respiratory diseases； It can also reduce the incidence of composite clinical events； and it demonstrates favorable safety profile.Keywords：Wenyangjiedu granules;severe coronavirus disease 2019 （COVID-19）;strengthening vital qi to eliminate pathogenic factor;randomised controlled trial;clinical efficacy76|112|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Clinical Efficacy of Yinxieping Tablets in Treatment of Psoriasis with Damp-heat Syndrome and Impact on PPARγ and STAT3 Enhanced Publication AI Introduction
Abstract：ObjectiveThis paper aims to observe the effects of Yinxieping Tablets on the expression of peroxisome proliferator-activated receptor γ （PPARγ） and signal transducer activator 3 （STAT3） in psoriasis patients with damp-heat syndrome and explore the mechanism in the treatment of psoriasis with damp-heat syndrome.MethodsA total of 47 subjects were included in this study， among whom 29 cases were in the psoriasis group and 18 cases were in the healthy control group. 17 cases with damp-heat syndrome and 12 cases without damp-heat syndrome were in the psoriasis group， and a self-controlled study was employed. The control group did not receive any oral medication， while the psoriasis group was administered Yinxieping tablets orally. After one month of treatment， the psoriasis area and severity index （PASI） scores before and after treatment were observed in both the damp-heat syndrome group and the non-damp-heat syndrome group. The efficacy rates and the levels of related factors were calculated.ResultsCompared to the healthy population， the PASI scores in both the damp-heat syndrome group and the non-damp-heat syndrome group decreased after treatment， with the efficacy rate in the damp-heat syndrome group being significantly higher than that in the non-damp-heat syndrome group （P<0.05）， which was statistically significant. Compared the non-damp-heat syndrome group， the contents of interleukin （IL）-17 and IL-23 in the damp-heat syndrome group significantly decreased after treatment （P<0.01）. Additionally， the mRNA expression level of PPARγ in the lesional tissue of the damp-heat syndrome group significantly increased， while that of STAT3 decreased （P<0.05）， with statistically significant differences.ConclusionYinxieping tablets can effectively alleviate the symptoms of psoriasis patients with damp-heat syndrome， upregulate the level of PPARγ in lesional tissue， and reduce the levels of STAT3 and serum factors such as IL-17 and IL-23， demonstrating definite clinical efficacy.Keywords：Yinxieping tablet;peroxisome proliferator-activated receptor γ （PPARγ）;signal transducer activator 3 （STAT3）;the psoriasis area and severity index （PASI） score;interleukin （IL）-17;IL-23;psoriasis96|312|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16- Abstract：ObjectiveTo construct a diagnostic-therapeutic model for community-acquired pneumonia （CAP） with pure Shaoyang syndrome and evaluate the clinical efficacy and safety of Xiao Chaihutang （XCHT） combined with conventional Western therapy.MethodsA randomized controlled trial design was adopted. Eighty CAP patients diagnosed with pure Shaoyang syndrome at Shenzhen Bao'an Traditional Chinese Medicine Hospital affiliated to Guangzhou University of Chinese Medicine from February to July 2024 were equally randomized to an observation group （n=40） and control group （n=40）. Ultimately， 76 patients （39 in the observation group and 37 in the control group） completed the trial. Both groups received conventional anti-infective therapy： ceftriaxone （2.0 g intravenous drip， once daily）， azithromycin （0.5 g intravenous drip， once daily for 3 days， then 0.5 g oral， once daily）， and ambroxol （30 mg intravenous push， twice daily）. The observation group additionally received XCHT. The treatment in both groups lasted for 10 days or until clinical recovery （with normal body temperature for ≥72 h， cough symptom score ≤ 3， and normal levels of inflammatory markers）. Primary outcomes included serum levels of inflammatory markers ［white blood cell count （WBC）， neutrophil count （NEUT）， high-sensitivity C-reactive protein （hs-CRP）， procalcitonin （PCT）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α）］， chest CT absorption rate， TCM symptom scores， cough symptom score， time to core symptom resolution （body temperature recovery， rales disappearance， and cough relief）， and hospital stay.ResultsNo severe adverse reactions occurred in either group. After treatment， the observation group showed reductions in serum levels of inflammatory markers （P<0.05）， cough symptom score （P<0.01）， scores of main TCM symptoms （cough， chest-hypochondrium fullness， fever-chill alternation， and sputum volume） and secondary symptoms （bitter taste， poor appetite， dry throat， and tongue manifestation）， and total symptom score （P<0.01）. The control group exhibited reductions in serum levels of inflammatory markers （P<0.05）， cough symptom score， TCM main/secondary symptom scores， and total symptom score （P<0.01）. The total response rate in the observation group was 89.74% （35/39）， which was higher than that （63.16%， 23/37） in the control group （χ2=9.279， P<0.05）. The observation group had shorter hospital stay ［（7.56±1.50） days vs （10.35±1.85） days］， time to rales disappearance ［（6.41±1.56） days vs. （8.92±1.87） days］， time to body temperature recovery ［（2.74±1.39） days vs. （4.30±1.51） days］， and time to cough relief ［（3.62±1.38） days vs. （6.97±1.95） days］ （P<0.001）. In addition， the observation group had lower levels of WBC， NEUT， CRP， PCT， IL-6， TNF-α （P<0.05）， lower scores of cough， chest-hypochondrium fullness， sputum volume， bitter taste， poor appetite， dry throat， and tongue manifestation， and lower total TCM symtom score （P<0.01）， and lower fever-chill alternation score （P<0.05）.ConclusionThe diagnostic-therapeutic model preliminarily established based on principal Shaoyang syndrome effectively intervened in the pathological progression of CAP. The classical formula XCHT， synergized with conventional Western anti-infective and expectorant therapy， significantly enhanced anti-inflammatory effects， accelerated the resolution of clinical symptoms， shortened hospital stays， and improved patient prognosis， with a good safety profile. This study provides a promising novel approach and preliminary evidence for the precision diagnosis and treatment of CAP combining Chinese and Western medicine， though the findings require further validation in larger-sample studies.Keywords：principal Shaoyang syndrome;community-acquired pneumonia;Xiao Chaihutang;diagnostic-therapeutic model;inflammatory cytokine70|95|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16
Role of Fluid Shear Stress in Pulmonary Fibrosis from Perspective of Lung Linking with All Vessels AI Introduction
Abstract：Pulmonary fibrosis （PF） is a fatal interstitial lung disease characterized by progressive pulmonary scarring and respiratory failure. Current Western medical treatments， such as nintedanib， are limited in their ability to reverse disease progression and are associated with notable adverse effects during long-term use. In traditional Chinese medicine （TCM）， PF is categorized under conditions such as lung atrophy （Fei Wei） and lung impediment （Fei Bi）， with its core pathogenesis attributed to deficiency of healthy Qi， obstruction of collaterals， and cumulative damage that is difficult to restore. In recent years， advances in biomechanical research have increasingly demonstrated that disturbances in fluid shear stress within the pulmonary microenvironment play a critical role in the initiation and progression of fibrosis. According to the TCM theory of lung linking with all vessels， this study systematically elucidates the intrinsic relationship between this classical theory and pulmonary biomechanical regulation from a multidisciplinary perspective. Our analysis suggests that under physiological conditions， appropriate fluid shear stress represents a micro-scale biomechanical manifestation of the lung's role in maintaining the dynamic balance of Qi and blood circulation. In PF， alveolar structural remodeling leads to local flow field disruption， and abnormally elevated or disordered shear stress promotes endothelial-to-mesenchymal transition and aberrant fibroblast activation， thereby accelerating excessive extracellular matrix deposition and disease progression. On this basis， we propose a pathophysiological evolution model characterized by abnormal descending and ascending of lung Qi （Qi）-abnormal mechanical output of lung collaterals （force）-Zang-Fu organ dysfunction. Furthermore， corresponding syndrome differentiation and therapeutic strategies are discussed with consideration to patterns such as Yin deficiency with lung dryness， lung Qi deficiency， lung-kidney Qi deficiency， as well as phlegm-dampness and blood stasis. From the perspective of Qi-collateral-force coupling， this study provides a novel theoretical framework for TCM interventions in PF and offers a reference for the modern biological interpretation and translational research of TCM theories.Keywords：pulmonary fibrosis;lung linking with all vessels;fluid shear stress;lung collaterals;biomechanics139|142|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Analysis and Evaluation of Animal Models of Acute Myocardial Infarction Based on Clinical Characteristics in Chinese and Western Medicine Enhanced Publication AI Introduction
Abstract：ObjectiveTo systematically evaluate the clinical concordance of existing animal models of acute myocardial infarction （AMI） based on the clinical characteristics of AMI in traditional Chinese medicine （TCM） and Western medicine， thus providing suggestions for constructing animal models that conform to the pathological features and TCM syndrome manifestations of AMI.MethodsThe articles related to animal models of AMI were retrieved from domestic and foreign databases such as China National Knowledge Infrastructure （CNKI）， Wanfang Data， and PubMed， with the time interval from January 2010 to January 2026. According to the domestic and international diagnostic criteria and guidelines for AMI and evaluation methods for animal models， this paper summarized， evaluated， and analyzed the clinical characteristics of AMI in TCM and Western medicine. From the pathological mechanisms in Western medicine and the TCM syndrome manifestations， a quantitative evaluation was conducted multiple types of models in terms of the modeling methods， mechanism characteristics， advantages and disadvantages， as well as the degree of concordance with clinical characteristics in both Western and TCM medicine.ResultsExisting animal models of AMI in Western medicine include ischemic， ischemia-reperfusion， chemically induced， cryoablation， hypoxia/reoxygenation， photochemical thrombosis， microembolism， metabolic + surgical， and gene engineering + surgical models. The animal models of AMI in TCM include models with Qi-Yin deficiency syndrome， deficiency-stasis-toxin syndrome， and blood stasis syndrome.ConclusionExisting animal models of AMI show high concordance with core Western medical indicators， but generally lack adequacy in simulating TCM syndrome patterns. They fail to effectively reproduce the holistic manifestation and dynamic evolution process of etiology-pathogenesis-syndrome. Future research should， on the basis of ensuring the stability and reliability of Western medical pathological models， integrate TCM etiological theories to construct a multi-dimensional animal model of AMI combining disease and syndrome. Additionally， an objective and quantified multi-dimensional evaluation system integrating Chinese and Western medicine should be established to promote the in-depth development of integrated Chinese and Western medicine research on AMI.Keywords：acute myocardial infarction;animal model;integration of Chinese and Western medicine;syndrome-disease integration;clinical concordance105|80|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Traditional Chinese Medicine Intervention Strategies for Diabetic Wound Healing Based on PI3K/Akt Signaling Pathway Enhanced Publication AI Introduction
Abstract：Diabetic wound （DW） is one of the serious complications of diabetes and has become a clinical challenge due to its protracted， refractory nature and high recurrence rate. The phosphatidylinositol 3 kinase/protein kinase B （PI3K/Akt） signaling pathway plays a core role in regulating cell proliferation， metabolism， apoptosis， and autophagy， and its functional inhibition is closely associated with impaired DW healing. Modern studies have demonstrated that dysfunction of this pathway can lead to overexpression of inflammatory factors， aggravated oxidative stress， increased apoptosis， and dysregulated autophagy， thereby delaying wound repair. Guided by the holistic concept and treatment based on pattern identification， traditional Chinese medicine （TCM） possesses the advantages of multi-component， multi-target， and holistic regulation. Numerous TCM monomers and compound formulas can regulate the PI3K/Akt signaling pathway， inhibit inflammatory signal transduction mediated by nuclear factor-κB （NF）-κB and others， enhance antioxidant enzyme activities， modulate the balance between apoptosis and autophagy， and promote the expression of vascular endothelial growth factor （VEGF） and other factors， thereby improving cellular functions in a high-glucose microenvironment and synergistically facilitating wound healing. Based on the TCM pathogenesis of "deficiency of vital Qi， stasis and toxin obstructing collaterals"， this paper proposes "reinforcing vital Qi and removing toxin， resolving stasis and dredging collaterals" as the core therapeutic principle for TCM intervention in DW， and summarizes that Chinese medicinals can multi-dimensionally regulate the PI3K/Akt signaling pathway through different treatment methods such as supplementing Qi and activating blood， warming Yang and dredging vessels， and clearing heat and removing toxin， embodying the unique advantage of TCM in "differentiation of disease and pattern， treatment of both the root cause and the manifestations". Future research should integrate systems pharmacology with clinical validation to deeply elucidate the mechanisms of multi-component synergistic regulation of the PI3K/Akt network by Chinese medicinals， providing more sufficient scientific evidence for the prevention and treatment of DW with TCM.Keywords：diabetic wounds;phosphatidylinositol 3 kinase/protein kinase B （PI3K/Akt） signaling pathway;traditional Chinese medicine intervention;multi-target therapy87|100|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16- Abstract：Stable chronic obstructive pulmonary disease （COPD） is a crucial stage for delaying the progression of the disease. Lung and kidney Qi deficiency is the core pathogenesis of stable COPD. The lung-tonifying and kidney-replenishing therapy has remarkable efficacy in treating stable COPD， with distinct characteristics. It can effectively alleviate the clinical symptoms of patients， reduce the frequency and severity of acute exacerbations， improve lung function and immune function， and enhance exercise tolerance and quality of life. In terms of the mechanism of action， numerous studies have shown that the lung-tonifying and kidney-replenishing formulas mainly exert therapeutic effects through regulating immune-inflammatory imbalance， antagonizing oxidative stress， correcting metabolic disorders， restoring protease/antiprotease imbalance， and regulating programmed cell death of alveolar epithelial cells， among other pathways. This paper reviews the ancient medical texts on lung distension and the academic experience of modern physicians to systematically summarize the current application status of the lung-tonifying and kidney-replenishing therapy in the clinical treatment of stable COPD and the biological mechanism it exerts through multiple pathways and multiple targets. However， existing studies often have problems such as short treatment courses， insufficient follow-up， and fragmented mechanism explanations. In the future， large-sample， long-term high-quality evidence-based studies should be conducted， and modern research technologies such as multi-omics， artificial intelligence， and microphysiological systems should be integrated to analyze the core components and action mechanisms of the lung-tonifying and kidney-replenishing formulas in the treatment of COPD through the "component-target-pathway" network. This will provide a high-quality evidence-based basis and innovative strategies for the prevention and treatment of COPD in the era of precision medicine， promoting the inheritance， innovation， and development of traditional Chinese medicine in this field.Keywords：chronic obstructive pulmonary disease;lung-tonifying and kidney-replenishing therapy;clinical application;mechanism of action;research progress101|101|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16
Research on Patterns of Syndrome Differentiation and Treatment for Lung Cancer Based on Case Reports： An Evidence-based Pathway Exploration for Complementing Clinical Guidelines Enhanced Publication AI Introduction
Abstract：ObjectiveCurrent clinical practice guidelines for traditional Chinese medicine （TCM） diagnosis and treatment of lung cancer lack a systematic pathway to integrate personalized clinical experience， which hinders the transformation of valuable knowledge from case reports into evidence-based evidence. This study aims to establish a standardized method to extract latent "formula-syndrome-efficacy" patterns from high-quality case reports， forming a structured evidence support pathway to supplement clinical guidelines with personalized treatment insights.MethodsWe systematically searched CNKI， Wanfang Data， VIP， CBM， PubMed， and Web of Science for case reports on TCM treatment for lung cancer published from inception to December 31， 2024， using relevant subject terms and keywords. Two researchers independently evaluated literature quality with a dedicated TCM case report scale. One hundred and two articles rated as "excellent" or "good" were included. We used Excel 2021 for herb frequency statistics and efficacy classification， SPSS Statistics 26.0 for systematic clustering analysis （Jaccard distance）， and SPSS Modeler 18.0 for association rule mining （confidence ≥80%， support ≥10%） to identify core herb pairs and compatibility rules， thereby refining the syndrome differentiation and treatment framework and clinical reasoning.Results1. Theoretical Origins： The analyzed cases primarily drew from classical texts such as the Huangdi's Internal Classic and the Required Readings from the Medical Ancestors， identifying internal deficiency allowing pathogen accumulation as the fundamental pathogenesis， with phlegm， stasis， and toxin aggregating on a foundation of healthy Qi deficiency. 2. Treatment Principles and Medication Patterns： ① The core medication principle was reinforcing healthy Qi to eliminate pathogens. High-frequency herbs included deficiency-tonifying herbs （e.g.， Astragali Radix and Atractylodis Macrocephalae Rhizoma）， phlegm-resolving and cough-relieving herbs （e.g.， Pinelliae Rhizoma and Fritillariae Thunbergii Bulbus）， and heat-clearing， detoxifying anticancer herbs （e.g.， Hedyotis diffusa and Scutellariae Barbatae Herba）. ② Core formulas followed two main strengthening approaches： replenishing Qi and invigorating the spleen to resolve phlegm （modified Liujunzi Tang） and replenishing Qi and nourishing Yin （modified Shashen Maidongtang）， often combined with herbs to harmonize the spleen and stomach （e.g.， Jiaosanxian）. ③ Concurrent deficiency and excess patterns predominated （79.76%）， most commonly dual deficiency of Qi and Yin accompanied by phlegm， stasis， and toxin， with herb selection adjusted accordingly. ④ Although the lung was central， the spleen was frequently involved， with herbs selected to support the spleen/lung axis （reinforcing earth to generate metal） and address phlegm at its source. ⑤ Insect and reptile medicinals were used cautiously， primarily for attacking pathogens and unblocking collaterals， and always combined with healthy Qi-replenishing herbs. 3. Diagnostic and Therapeutic Characteristics： Distinctive theories like cancer toxin metastasis， cancerous turbidity， and promoting Yin to limit Yang were extracted， with corresponding methods like purging Fu-organs to drain the lung， consolidating the root and clearing the source， and syndrome-specific strategies for complications and adverse effects of modern therapies.ConclusionThis systematic integration of high-quality TCM lung cancer case reports provides crucial supplements to current guidelines： 1. It refines the core diagnostic framework， confirming dual deficiency of Qi and Yin as the root， with intermingled phlegm， stasis， and toxin as the manifestation as the most prevalent clinical syndrome. 2. It offers an operational atlas of common formulas and herb combinations， revealing high-frequency patterns centered on replenishing Qi and invigorating the spleen to resolve phlegm， and supplementing Qi and nourishing Yin， while integrating anticancer detoxification and spleen-stomach protection. 3. It enriches guidelines with specific strategies for complex scenarios， extracting distinctive theories like cancer toxin metastasis and systematic approaches for managing complications. This study pioneers a methodology to transform narrative case reports into structured， practice-based evidence， informing the dynamic updating of clinical guidelines with real-world clinical wisdom.Keywords：lung cancer;traditional Chinese medicine case report;pattern of syndrome differentiation and treatment;evidence83|116|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Differentiation and Treatment of Vulnerable Atherosclerotic Plaque Based on "Collateral Disease" Theory Enhanced Publication AI Introduction
Abstract：The rupture of vulnerable atherosclerotic plaques is the major pathological mechanism underlying acute adverse cardiovascular events. Abundant pathological neovascularization within plaques is an important factor contributing to plaque instability. Therefore， inhibiting pathological angiogenesis may represent an effective strategy for stabilizing vulnerable plaques. The theory of collateral disease is an important component of the theoretical system of traditional Chinese medicine （TCM） and provides guidance for the prevention and treatment of microvascular disorders. Based on the theory of collateral disease， this study explored， from a microscopic perspective， the commonalities between collaterals and physiological neovessels in terms of anatomical structure and physiological function， and investigated the similarities in pathological characteristics between diseased collaterals and pathological neovascularization. Taking these similarities as the point of entry， this study integrates TCM theory with modern medicine to interpret the mechanisms by which pathological neovascularization and abnormal hemodynamics contribute to plaque vulnerability， and discusses the scientific connotations of the core pathogenesis of vulnerable atherosclerotic plaques， namely "heart Qi deficiency and collateral obstruction due to blood stasis". Focusing on this core pathogenesis， the therapeutic principle of "dredging and supplementing in the treatment of collateral diseases" is proposed， together with the therapeutic approach of "promoting blood circulation and dredging collaterals while replenishing qi and facilitating collateral flow". In addition， the study investigates the mechanisms by which single Chinese herbs and herbal compound formulas prevent and treat vulnerable atherosclerotic plaques through the multi-target regulation of pathological neovascularization， and analyzes the theoretical convergence between TCM and Western medicine， with the aim of providing new insights into the prevention and treatment of vulnerable atherosclerotic plaques.Keywords：atherosclerosis;the theory of collateral disease;dredging and supplementing in the treatment of collateral diseases136|114|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16- Abstract：Ulcerative colitis （UC） is a subtype of inflammatory bowel disease， and the lesion primarily affects the colon and rectum. Its typical clinical manifestations include abdominal pain， diarrhea， and mucopurulent bloody stools. The pathogenesis of UC remains not fully understood but is closely associated with genetic susceptibility， immune dysregulation， and intestinal microecological imbalance. Mitophagy is a process that maintains intracellular mitochondrial health by clearing damaged mitochondria. Ferroptosis is a type of regulated cell death controlled by genetic coding， usually accompanied by significant iron accumulation and excessive lipid peroxidation. Mitophagy is a key factor mediating the inflammatory response induced by ferroptosis. Insufficient mitophagy， excessive reactive oxygen species （ROS） production， and iron metabolism disorders trigger ferroptosis， further leading to the accumulation of pathological products and the progression of UC. Energy deficiency caused by insufficient mitophagy， ferroptosis-driven inflammatory response， and accumulation of pathological products intrinsically align with the traditional Chinese medicine theory of "deficient Qi induced stagnation". Taking this theory as a starting point， this paper elucidated the intrinsic connection between mitophagy-mediated ferroptosis and "deficient Qi induced stagnation" and explored the intrinsic connection between traditional Chinese medicine theory and the regulation of UC pathogenesis in this process. This study is expected to systematically explain the modern biological mechanisms of traditional Chinese medicine in intervening in UC.Keywords：ulcerative colitis;mitophagy;ferroptosis;deficient Qi induced stagnation;traditional Chinese medicine107|109|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16
Treatment of Insomnia by Traditional Chinese Medicine Through Regulating Brain Neurotransmitters： A Review AI Introduction
Abstract：Insomnia， as a global public health issue， has seen its incidence rate increasing year by year with the rise of social pressure. Modern medical research indicates that neurotransmitter imbalance is one of the core pathological mechanisms of insomnia， involving multiple neurotransmitters such as γ-aminobutyric acid （GABA）， glutamate （Glu）， serotonin （5-HT）， dopamine （DA）， and norepinephrine （NE）. Currently， although common clinical chemical drugs such as benzodiazepine receptor agonists can improve symptoms in the short term， long-term use easily leads to problems such as tolerance， dependence， and cognitive function impairment. In contrast， traditional Chinese medicine， relying on an integrated regulatory model of "multiple components， multiple targets， and multiple pathways"， has demonstrated unique advantages in restoring neurotransmitter balance and improving sleep quality， gradually becoming a research hotspot. This paper reviewed the recent research progress on the treatment of insomnia by traditional Chinese medicine through regulating brain neurotransmitters. First， it introduced the relationship between insomnia and neurotransmitter imbalance， including the action mechanisms of neurotransmitters such as GABA， Glu， 5-HT， NE， and DA in insomnia. Then， it elaborated on the regulatory effects of traditional Chinese medicine compounds and monomers on these neurotransmitters. For example， Suanzaoren decoction improves sleep quality by enhancing GABAergic effects. Chaihu Shugan Powder exerts therapeutic effects by regulating the GABA/Glu balance. Huanglian Ejiao Decoction ameliorates insomnia symptoms by regulating 5-HT and NE levels. Additionally， the therapeutic effects and action mechanisms of traditional Chinese medicine compounds such as Jiaotai Pill， Baihe Dihuang Decoction， and Longdan Xiegan Decoction on insomnia were summarized. Studies show that traditional Chinese medicine compounds and monomers significantly improve sleep quality in insomnia patients by synergistically regulating neurotransmitter networks through multiple targets， with significantly lower recurrence rates and incidences of adverse reactions compared to conventional western medicines. Although the action mechanisms of traditional Chinese medicine in regulating neurotransmitters for insomnia treatment have been partially understood， there are still some problems requiring further exploration， such as limited exploration on transmitter pathways such as cholinergic and histaminergic， as well as the need to strengthen studies on the target specificity of traditional Chinese medicine monomer components. In the future， randomized controlled trials with multiple centers and large samples can be conducted， and the long-term efficacy and safety of traditional Chinese medicine compounds can be verified by combining the trials with biomarkers.Keywords：insomnia;traditional Chinese medicine;neurotransmitter;γ-aminobutyric acid （GABA）;5-hydroxytryptamine159|148|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Traditional Chinese Medicine Intervening Signaling Pathways Related to Type 2 Diabetes Mellitus Complicated with Hyperlipidemia： A Review Enhanced Publication AI Introduction
Abstract：Type 2 diabetes mellitus is a common endocrine syndrome characterized by glucose metabolism disorders， often accompanied by lipid metabolism dysfunction and complicated with hyperlipidemia. The etiology of type 2 diabetes mellitus has not been fully elucidated， but insulin resistance and pancreatic β-cell dysfunction play central roles in its pathophysiology. Insulin resistance is the shared pathological basis of these two diseases. An imbalance in insulin function directly disrupts lipid metabolic order， thereby inducing hyperlipidemia. Modern medical treatments primarily target regulating laboratory indicators. While this approach yields certain therapy to some extent， it is associated with unstable efficacy， frequent adverse reactions， and a high recurrence rate， which imposes a heavy burden on patients. In recent years， traditional Chinese medicine has achieved notable progress in the treatment of type 2 diabetes mellitus complicated with hyperlipidemia. Traditional Chinese medicine exhibits distinct advantages， including multi-targeted and multi-pathway actions， simplicity， high efficacy， cost-effectiveness， and minimal side effects in intervening type 2 diabetes mellitus complicated with hyperlipidemia. Numerous studies have demonstrated that traditional Chinese medicine components （e.g.， traditional Chinese medicine-derived extracellular vesicles） and traditional Chinese medicine compound formulae can modulate the signaling pathways related to disease to regulate insulin sensitivity， lipid metabolism， inflammatory responses， endoplasmic reticulum stress， gut microbiota， and energy homeostasis， thereby ameliorating glucose-lipid metabolic disorders and delaying disease progression. Therefore， this review summarized the key signaling pathways targeted by traditional Chinese medicine in intervening type 2 diabetes mellitus complicated with hyperlipidemia， including the insulin receptor substrate/phosphatidylinositol-3-kinase/protein kinase B （IRS/PI3K/Akt） signaling pathway， adenosine monophosphate-activated protein kinase （AMPK） signaling pathway， peroxisome proliferator-activated receptors （PPARs） signaling pathway， the nuclear factor kappa B/c-Jun N-terminal kinase （NF-κB/JNK） signaling pathway， protein kinase RNA-like endoplasmic reticulum kinase （PERK） signaling pathway， the short-chain fatty acid/glucagon-like peptide-1 （SCFAs/GLP-1） signaling pathway， Wingless/Int-1 （Wnt） signaling pathway， the protein kinase C （PKC） signaling pathway， and sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator-1alpha （SIRT1/PGC-1α） signaling pathway， aiming to provide a reference direction for the research and development of novel drugs.Keywords：traditional Chinese medicine;type 2 diabetes mellitus;hyperlipidemia;signaling pathway;mechanism of action124|122|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Effect and Mechanisms of Traditional Chinese Medicine in Intervening Wound Healing Based on TGF-β/Smad Signaling Pathway：A Review Enhanced Publication AI Introduction
Abstract：Wound healing is a dynamic repair process involving the coordinated participation of multiple cell types， active factors， and signaling networks following tissue injury. In clinical practice， issues such as slow healing progress， persistent non-closure of wounds， and pathological scar formation significantly impair patients' quality of life. Therefore， optimizing healing time and repair quality has become a key focus of clinical research. Current clinical treatments have limitations， including limited efficacy， high cost， high recurrence rates， and excessive pathological scar hyperplasia， highlighting the urgent need for novel intervention strategies. In recent years， with deepening research into the mechanisms of wound healing， the transforming growth factor-β （TGF-β）/Smad signaling pathway， a core pathway regulating fibroblast activation， collagen synthesis， and tissue remodeling， is crucial for maintaining the dynamic balance of wound healing. It can modulate the resolution of inflammation， angiogenesis， and collagen metabolism through stage-specific control of gene transcription， thereby exerting bidirectional regulatory effects during the inflammatory， proliferative， and remodeling phases of wound healing. Traditional Chinese medicine， with its unique advantages of multiple targets， pathways， and mechanisms， can accelerate wound healing and inhibit excessive scar formation by targeting key molecules of the TGF-β/Smad signaling pathway. This article systematically reviewed the mechanisms by which the TGF-β/Smad signaling pathway regulates wound healing， covering four aspects： inflammation and oxidative stress， angiogenesis， apoptosis， and epithelial-mesenchymal transition （EMT）. It also summarized the single herbs， active components of traditional Chinese medicine， herb pairs of traditional Chinese medicine， and formulas that modulate this pathway， aiming to fully exploit the advantages of traditional Chinese medicine in the field of wound healing and provide new ideas for clinical research and new drug development for wound healing.Keywords：traditional Chinese medicine;active component;wound healing;transforming growth factor-β （TGF-β）/Smad signaling pathway181|433|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16Traditional Chinese Medicine Treating Depression Through Inhibiting NLRP3 Inflammasome Pathway： A Review Enhanced Publication AI Introduction
Abstract：Depression is one of the most burdensome mental disorders worldwide. Conventional Western medicines， such as selective serotonin reuptake inhibitors， have limitations including delayed onset of action， high relapse rate after drug withdrawal， and multiple adverse reactions. In recent years， studies have confirmed that the neuroinflammatory cascade mediated by the NOD-like receptor protein 3 （NLRP3） inflammasome is a key mechanism in the occurrence and development of depression. Its excessive activation promotes the release of pro-inflammatory cytokines， leading to neuronal damage， decreased synaptic plasticity， and neuroendocrine disorders. Therefore， inhibiting excessive activation of the NLRP3 inflammasome has become an important target for researching and developing novel antidepressants. This article systematically reviewed the research progress on active components of traditional Chinese medicine， single herbs of traditional Chinese medicine， and traditional Chinese medicine compound prescriptions in improving depression by regulating the NLRP3 inflammasome pathway. It focused on analyzing their multi-modal mechanisms of action， including inhibiting NLRP3 assembly and activation to alleviate neuroinflammation， blocking caspase-1/gasdermin D （GSDMD）-mediated pyroptosis， regulating the nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） pathway to enhance antioxidant stress， reestablishing hypothalamic-pituitary-adrenal （HPA） axis homeostasis， improving monoamine neurotransmitter balance， and upregulating brain-derived neurotrophic factor （BDNF） expression. By summarizing the unique advantages of traditional Chinese medicine in regulating the NLRP3 inflammasome through multiple components and targets， this article provides a theoretical reference and scientific basis for the modernized research of traditional Chinese medicine in antidepressant therapy and the development of innovative drugs.Keywords：depression;NOD-like receptor protein 3（NLRP3） inflammasome;antioxidation;neuroinflammation;traditional Chinese medicine;active components107|96|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16- Abstract：Diabetic kidney disease （DKD） is one of the most common and destructive chronic complications of diabetes. Although conventional therapies can delay disease progression through glycemic control， as well as the inhibition of inflammation， fibrosis， the renin-angiotensin system， and other targets， they are still unable to halt deterioration throughout the entire course of DKD. In recent years， the gut microbiota-microbial metabolite-mitochondrial axis has been proposed as an important framework for understanding the novel pathological mechanisms underlying DKD. By reviewing the relevant literature in China and other countries， this paper found that gut microbiota dysbiosis led to reduced short-chain fatty acids （SCFAs）， disordered bile acids （BAs）， and increased indole derivatives and uremic toxin precursors. These relevant metabolites act on the kidney through the circulation， induce mitochondrial structural and functional damage， and subsequently trigger energy metabolism disorders， oxidative stress， inflammatory responses， and impaired mitophagy， thereby promoting DKD progression. Traditional Chinese medicine may exert synergistic intervening effects by regulating gut microbiota structure， suppressing inflammation and oxidative stress， improving intestinal mucosal barrier function， correcting metabolite abnormalities， and maintaining mitochondrial homeostasis. This paper summarized the characteristics of gut microbiota and metabolic disorders related to DKD， the key links of mitochondrial damage， and their coupled mechanisms. However， current research still mainly focuses on correlational evidence and verification of the causal chain linking metabolites， receptors， and mitochondrial function remains insufficient. Future research should further clarify the specific mechanisms of action by integrating approaches such as gut microbiota depletion and reconstruction， fecal microbiota transplantation， metabolite supplementation， and receptor blockade， providing a reference for the systematic research and clinical translation of traditional Chinese medicine in the prevention and treatment of DKD.Keywords：diabetic kidney disease;gut microbiota;gut-kidney axis;microbial metabolite;mitochondrion;traditional Chinese medicine119|107|0<HTML><H-PDF> <L-PDF>Updated：2026-07-16
