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Online FirstList of IssuesDocument Types
Effect of Modified Baoyuantang Combined with Linggui Zhugantang on Myocardial Mitochondrial Damage and NLRP3/GSDMD-mediated Pyroptosis in Rat Model of Post-myocardial Infarction Heart Failure Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the therapeutic effects of modified Baoyuantang combined with Linggui Zhugantang on post-myocardial infarction heart failure in rats and its influence on NOD-like receptor pyrin domain-containing protein 3 （NLRP3）/gasdermin D （GSDMD）-mediated pyroptosis.MethodsSixty male SD rats were randomized into sham， model， low-， medium-， and high-dose （2.52， 5.04， 10.08 g·kg-1， respectively） modified Baoyuantang combined with Linggui Zhugantang， and sacubitril/valsartan sodium （0.021 g·kg-1） groups， with 10 rats in each group. Except the sham group， the other groups underwent left anterior descending coronary artery ligation for the modeling of myocardial infarction. The treatment groups were administrated with corresponding drugs by gavage， and the sham and model groups received an equal volume of normal saline. Administration began on the first day after successful modeling， once daily， for 4 weeks. Echocardiography was used to measure left ventricular ejection fraction （LVEF）， left ventricular fractional shortening （LVFS）， left ventricular end-diastolic and end-systolic diameters （LVIDd and LVIDs）， left ventricular posterior wall thicknesses at end-diastole and end-systole （LVPWd， LVPWs）， and left ventricular volumes at end-diastole and end-systole （LV Vold and LV Vols）. Cardiac mass index and heart weight-to-tibia length ratio were calculated. Hematoxylin-eosin （HE） staining and Sirius Red staining were performed to observe myocardial morphology and collagen deposition. Immunohistochemistry was employed to detect the expression of type I collagen （Collagen Ⅰ）， NLRP3， GSDMD， and interleukin-1β （IL-1β）. Transmission electron microscopy was used to observe the mitochondrial ultrastructure. Tetramethylrhodamine methyl ester （TMRM） staining was conducted to assess mitochondrial membrane potential （MMP） in cardiomyocytes. Real-time PCR was used to quantify the mRNA levels of NLRP3， cysteinyl aspartate-specific proteinase-1 （Caspase-1）， IL-1β， GSDMD， and interleukin-18 （IL-18） in the myocardial tissue. Western blotting was employed to determine the protein levels of NLRP3， Caspase-1， GSDMD， IL-1β， IL-18， nuclear factor kappa-B （NF-κB） p50， and NF-κB p65 in the myocardial tissue. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the serum levels of tumor necrosis factor-α （TNF-α）， IL-1β， and IL-6.ResultsCompared with the sham group， the model group showed increased LVIDd， LVIDs， LV Vold， LV Vols， cardiac mass index， and heart weight-to-tibia length ratio （P<0.05）， decreased LVPWs， LVEF， LVFS， and MMP （P<0.05）， evident myocardial inflammation， fibrosis， and mitochondrial damage， upregulated expression of NLRP3， Caspase-1， GSDMD， IL-1β， IL-18， NF-κB p50， and NF-κB p65， and elevated serum levels of TNF-α， IL-1β， and IL-6 （P<0.05）. Compared with the model group， modified Baoyuantang combined with Linggui Zhugantang reduced the LVIDd， LVIDs， LV Vols， cardiac mass index， and heart weight-to-tibia length ratio （P<0.05）， increased the LVPWs， LVEF， LVFS， and MMP （P<0.05）， alleviated myocardial inflammation and fibrosis， improved the mitochondrial structure and function， downregulated the expression of NLRP3， Caspase-1， GSDMD， IL-1β， IL-18， NF-κB p50， and NF-κB p65 （P<0.05）， and reduced the serum levels of TNF-α， IL-1β， and IL-6 （P<0.05）.ConclusionModified Baoyuantang combined with Linggui Zhugantang can ameliorate post-myocardial infarction ventricular remodeling and improve the cardiac function by reducing mitochondrial damage and inhibiting NLRP3/GSDMD-mediated pyroptosis.Keywords：Baoyuantang;Linggui Zhugantang;myocardial infarction;heart failure;pyroptosis215|84|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Exploring Mechanism of Xiaojinwan-containing Serum in Inhibiting Breast Cancer Cells Based on Wnt/β-catenin Signaling Pathway AI Introduction
Abstract：ObjectiveTo investigate the role and underlying mechanism of the Wnt/β-catenin signaling pathway in the process of Xiaojinwan （XJW）-containing serum interfering with endothelial-mesenchymal transition （EMT） in human breast cancer MDA-MB-231 cells.MethodsXJW-containing serum was prepared by intragastric administration of XJW （4 g·kg-1） to SD rats. MDA-MB-231 cells were cultured in vitro. β-Catenin overexpression and knockdown plasmids were constructed and transfected into MDA-MB-231 cells. The optimal XJW-containing serum （4 g·kg-1） according to previous studies was used for β-catenin intervention and overexpression experiments. The groups for intervention/overexpression experiments included intervention/overexpression blank group， β-catenin intervention/overexpression group， intervention/overexpression blank + XJW group， and β-catenin intervention/overexpression + XJW group. Cell morphology was observed under a microscope. Flow cytometry was used to detect and record apoptosis rates. Western blot was performed to measure apoptosis-related proteins ［B-cell lymphoma 2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and active-Caspase-3］ and EMT-related proteins （E-cadherin， N-cadherin， and vimentin）. Real-time polymerase chain reaction （Real-time PCR） was used to detect β-catenin mRNA expression levels in different groups.ResultsIntervention experiment results showed that compared with the intervention blank group， the β-catenin intervention group and the intervention blank + XJW group showed increased apoptosis rates （P<0.05， P<0.01）， elevated protein levels of Bax， active Caspase-3， and E-cadherin （P<0.05， P<0.01）， and decreased protein levels of Bcl-2 and Vimentin （P<0.05， P<0.01）. β-catenin mRNA expression was reduced in the β-catenin intervention group （P<0.05， 0.63 ± 0.15） and the intervention blank + XJW group （P<0.05， 0.79 ± 0.33）. Compared with the β-catenin intervention group， the β-catenin intervention + XJW group exhibited an increased apoptosis rate （P<0.01）， elevated Bax and active Caspase-3 protein levels （P<0.05， P<0.01）， and decreased Bcl-2， N-cadherin， and Vimentin protein levels （P<0.05）. β-catenin mRNA expression was further reduced in the β-catenin intervention + XJW group （P<0.01， 0.22 ± 0.08）. Compared with the intervention blank + XJW group， the β-catenin intervention + XJW group showed an increased apoptosis rate （P<0.01）， elevated Bax， active Caspase-3， and E-cadherin protein levels （P<0.05， P<0.01）， and decreased Bcl-2， N-cadherin， and vimentin protein levels （P<0.05， P<0.01）. β-catenin mRNA expression was also reduced （P<0.05）. Overexpression experiment results showed that compared with the overexpression blank group， the β-catenin overexpression group exhibited a reduced apoptosis rate （P<0.01）， while the overexpression blank + XJW group showed an increased apoptosis rate （P<0.05）. In the β-catenin overexpression and β-catenin overexpression + XJW groups， Bax and E-cadherin protein levels decreased （P<0.05， P<0.01）， while Bcl-2， N-cadherin， and vimentin levels increased （P<0.05）. In the overexpression blank + XJW group， Bax and E-cadherin levels increased （P<0.05， P<0.01）， while Bcl-2， N-cadherin， and vimentin levels decreased （P<0.05， P<0.01）. β-catenin mRNA expression increased in the β-catenin overexpression group （P<0.01， 7.26 ± 1.03） but decreased in the overexpression blank + XJW group （P<0.05， 0.73 ± 0.14）. Compared with the β-catenin overexpression group， the β-catenin overexpression + XJW group showed an increased apoptosis rate （P<0.01）， elevated Bax and E-cadherin levels （P<0.05）， and decreased N-cadherin and vimentin levels （P<0.05）. β-catenin mRNA expression was reduced （P<0.05， 4.65 ± 1.02）. Compared with the overexpression blank + XJW group， the β-catenin overexpression + XJW group exhibited a reduced apoptosis rate （P<0.01）， decreased Bax and E-cadherin levels （P<0.01）， and increased Bcl-2， N-cadherin， and Vimentin levels （P<0.05）. β-catenin mRNA expression increased （P<0.01）.ConclusionXJW-containing serum inhibits breast cancer cell proliferation by suppressing EMT， which is associated with the regulation of the Wnt/β-catenin pathway.Keywords：Xiaojinwan-containing serum;MDA-MB-231 cells;epithelial-mesenchymal transition（EMT）;Wnt/β-catenin signaling pathway;mechanism170|138|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Si Junzitang Ameliorates Alzheimer's Disease by Regulating Keap1/Nrf2/HO-1 Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo explore the mechanisms through which Si Junzitang （SJZD） ameliorates Alzheimer's disease （AD） induced by scopolamine （SCOP） in mice and the PC12 cell model induced by H2O2 based on the Kelch-like ECH-associated protein 1 （Keap1）/nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway.MethodsIn the animal experiments， an AD model was established in mice by intraperitoneal injection of SCOP （3 mg·kg-1）. Morris water maze and open field tests （OFT） were conducted to assess learning and memory abilities. Hematoxylin-eosin （HE） staining and Nissl staining were performed to observe pathological changes in neurons. Immunofluorescence was used to detect amyloid β-protein1-42 （Aβ1-42） expression， and immunohistochemistry was employed to detect phosphorylated （p）-Tau expression. Transmission electron microscopy （TEM） was employed to observe ultrastructural changes in hippocampal neurons and synapses. Biochemical methods were used to measure the levels of acetylcholine （ACh）， acetylcholinesterase （AChE）， superoxide dismutase （SOD）， malondialdehyde （MDA）， catalase （CAT）， and lactate dehydrogenase （LDH）. Real-time PCR and Western blot were employed to measure the mRNA and protein levels of molecules in the Keap1/Nrf2/HO-1 pathway in the hippocampus. In the cell experiments， a PC12 cell model of oxidative damage model was established with H2O2. Cell count kit-8 （CCK-8） assays and flow cytometry were adopted to measure cell viability and apoptosis rates， and Western blot was employed to quantify the expression levels of proteins in the Keap1/Nrf2/HO-1 pathway.ResultsThe animal experiments showed that compared with the model group， the SJZD and donepezil groups showed shortened escape latency （P<0.01）， increased time in the target quadrant and platform crossings， and increased movement distance and duration in the central area of the open field （P<0.05， P<0.01）. HE and Nissl staining showed more organized neurons and increased Nissl bodies in the drug intervention groups （P<0.05， P<0.01）， and the Aβ1-42 and p-Tau expression levels were downregulated （P<0.05， P<0.01）. TEM revealed reduced ultrastructural damage in hippocampal neurons and synapses in the drug intervention groups. In addition， the drug intervention groups showed declined levels of MDA， LDH， and AChE （P<0.05， P<0.01）， elevated levels of SOD， CAT， and ACh （P<0.05， P<0.01）， reduced Keap1 expression and increased Nrf2， HO-1， and NQO1 expression in the hippocampus （P<0.05， P<0.01）. The cell experiments showed that compared with the model group， the SJZD-containing serum increased the cell viability （P<0.05， P<0.01）， and decreased total apoptosis rates （P<0.05， P<0.01）. The drug intervention groups showed upregulated protein levels of Nrf2 and HO-1 and downregulated protein level of Keap1 （P<0.05， P<0.01）.ConclusionSJZD demonstrates protective effects against SCOP-induced AD in mice and H2O2-induced damage in PC12 cells through antioxidant mechanisms mediated by the Keap1/Nrf2/HO-1 pathway.Keywords：Si Junzitang;Alzheimer's disease;oxidative stress;Kelch-like ECH-associated protein 1 （Keap1）/nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway228|69|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Mechanisms of Shangxia Liangji Danin Improving Cognitive Function in AD Mice Based on PI3K/Akt Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the mechanisms by which Shangxia Liangji pills improve cognitive function in Alzheimer's disease （AD） mice based on the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） pathway， aiming to provide experimental evidence for its clinical use in AD treatment.MethodsFifty APP/PS1 double-transgenic mice were randomly divided into a model group， Shangxia Liangji pills low-dose group， medium-dose group， high-dose group， and donepezil hydrochloride group， with 10 mice in each group. Additionally， 10 C57BL/6 mice of the same genetic background were assigned to the normal group. Cognitive function was assessed using the Morris water maze and novel object recognition tests. Hippocampal pathological changes were observed using transmission electron microscopy and Nissl staining. Neuroinflammation in hippocampal tissue was detected by enzyme-linked immunosorbent assay （ELISA）. Protein expression levels of PI3K/Akt pathway-related proteins， postsynaptic density protein 95 （PSD95）， and amyloid precursor protein （APP） in hippocampal tissue were measured by Western blot.ResultsCompared with the normal group， the model group exhibited significantly increased total swimming distance and escape latency， significantly reduced number of platform crossings （P<0.01）， and a decreased recognition index （P<0.01）. Marked neuronal apoptosis was observed in the hippocampal region， with a marked reduction in the number of neurons in the CA3 region （P<0.01）. Levels of interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in hippocampal tissue were significantly elevated （P<0.01）. APP expression in hippocampal tissue was markedly upregulated （P<0.01）， while PSD95， p-PI3K/PI3K， and p-Akt/Akt protein expression were significantly downregulated （P<0.01）. Compared with the model group， the Shangxia Liangji pills high-dose group showed significantly reduced total swimming distance and escape latency， significantly increased number of platform crossings （P<0.01）， and an elevated recognition index （P<0.01）. Hippocampal neuronal apoptosis was alleviated， with a significant increase in the number of neurons in the CA3 region （P<0.01）. Levels of IL-6， IL-1β， and TNF-α were significantly decreased （P<0.01）. APP expression was downregulated （P<0.05）， while PSD95， p-PI3K/PI3K， and p-Akt/Akt protein expression were significantly upregulated （P<0.01）.ConclusionShangxia Liangji pills may improve cognitive function in AD mice by modulating the PI3K/Akt pathway， thereby reducing neuroinflammation and alleviating neuronal and synaptic injury.Keywords：Shangxia Liangji pills;Alzheimer's disease;phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway90|60|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Mechanism of Gancao Fuzitang Improving Knee Osteoarthritis in Rats via Regulating PI3K/Akt/mTOR Signaling Pathway and Promoting Autophagy Enhanced Publication AI Introduction
Abstract：ObjectiveThis paper aims to investigate the intervention effect and molecular mechanism of Gancao Fuzitang （GCFZT） in knee osteoarthritis （KOA）.MethodsNetwork pharmacology was employed to predict the key targets and signaling pathways of GCFZT. Fifty SD rats were randomly divided into a sham group， a model group （KOA）， a low-dose GCFZT group （GCFZT-L， 2.8 g·kg-1）， a high-dose GCFZT group （GCFZT-H， 5.6 g·kg-1）， and a positive drug celecoxib group （Celecoxib， 20 mg·kg-1）， with 10 rats in each group. The rats in the sham group and the model group were given an equal volume of distilled water. Except for the sham group， the other four groups underwent anterior cruciate ligament transection to establish the KOA rat model. After successful modeling， the rats in each group received intragastric administration once a day for eight consecutive weeks. The structural changes of cartilage and subchondral bone were assessed via micro-computed tomography （micro-CT） and histological staining. The levels of inflammatory factors in the serum， such as interleukin-1β （IL-1β）， IL-6， and tumor necrosis factor-α （TNF-α） were measured using an enzyme linked immunosorbent assay （ELISA） kit. Real-time quantitative polymerase chain reaction （Real-time PCR）， Western blot， and immunohistochemistry were used to detect changes in the expression of autophagy-related proteins such as microtubule-associated protein 1 light chain 3B （LC3B）， selective autophagy junction protein 62 （p62）， and autophagy key molecule yeast Atg6 homolog （Beclin-1） in articular cartilage， as well as key molecules of the phosphatidylinositol 3 kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway.ResultsNetwork pharmacology analysis suggests that GCFZT may exert anti-osteoarthritic effects through regulating the PI3K/Akt/mTOR pathway. In vivo experiment shows that GCFZT can significantly improve cartilage degeneration and attenuate subchondral bone destruction in KOA rats. Detection results of inflammatory factors in the serum reveal that， compared with those in the sham group， the levels of IL-6， IL-1β， and TNF-α in the serum of rats in the KOA group are significantly increased （P<0.05）. Compared with those in the KOA group， the levels of these three inflammatory factors in the GCFZT-L， GCFZT-H， and Celecoxib groups were significantly decreased （P<0.05）. However， there was no statistically significant difference in these three inflammatory factor levels between the GCFZT-H group and the celecoxib group. These findings suggest that GCFZT can effectively inhibit the systemic inflammatory response in KOA rats. Mechanism research indicates that GCFZT inhibits activation of the PI3K/Akt/mTOR pathway， thereby enhancing autophagic activity and improving chondrocyte function and matrix degeneration.ConclusionGCFZT improves cartilage and subchondral bone damage in KOA rats by inhibiting the PI3K/Akt/mTOR signaling pathway and promoting autophagy. These findings provide theoretical evidence for the application of GCFZT in the prevention and treatment of osteoarthritis.Keywords：Gancao Fuzitang;knee osteoarthritis;phosphatidylinositol 3 kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR）;autophagy;inflammation65|57|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Mechanisms of Dahuang Gancaotang in Improving Ferroptosis in Chronic Kidney Disease through SIRT3-mediated Deacetylation of p53 AI Introduction
Abstract：ObjectiveTo investigate the mechanisms by which Dahuang Gancaotang （DHGC） alleviates ferroptosis in chronic kidney disease （CKD） via silent information regulator 3 （SIRT3）-mediated deacetylation of tumor protein p53 （p53）.MethodsIn vivo， a CKD mouse model was established by feeding a 0.2% adenine-containing diet. Seventy-two C57BL/6 mice were randomly divided into six groups： blank group， model group， DHGC low-， medium-， and high-dose groups （0.975， 1.95， 3.90 g·kg-1）， and valsartan group （0.025 g·kg-1）， with 12 mice in each group. Renal function was evaluated by measuring serum blood urea nitrogen （BUN） and creatinine （SCr）. Renal pathological changes were assessed using hematoxylin-eosin （HE）， periodic acid-Schiff （PAS）， and Masson staining. Immunohistochemistry was used to detect the expression of collagen type （Col）Ⅰ， ColⅢ， and α-smooth muscle actin （α-SMA） in renal tissue to evaluate renal fibrosis. Enzyme-linked immunosorbent assay （ELISA） was used to measure serum tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） to assess inflammatory responses. Colorimetric assays were used to determine superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione （GSH）， and renal total iron content to evaluate lipid peroxidation and iron metabolism. Western blot was used to detect the protein expression of the SIRT3/p53 signaling pathway， acetylated p53 （ac-p53）， and glutathione peroxidase 4 （GPX4） in renal tissue. In vitro， a ferroptosis model of HK-2 cells was induced using erastin. Cells were divided into six groups： blank group， model group， DHGC-containing serum low-， medium-， and high-dose groups （15 rats were randomly divided into three groups， n = 5 per group， and gavaged with 0.675， 1.35， 2.70 g·kg-1 to prepare medicated serum）， and ferrostatin-1 （Fer-1） group （5 μmol·L-1）. The cell counting Kit-8 （CCK-8） assay was used to determine cell viability and to screen the optimal concentrations of erastin and DHGC-containing serum. Western blot was used to detect SIRT3/p53 pathway proteins， ac-p53， and GPX4 expression. Immunofluorescence confocal microscopy was used to observe p53 nuclear translocation.ResultsIn vivo， compared with the blank group， the model group showed significantly increased BUN and SCr levels （P<0.01）. Severe renal pathological injury and aggravated renal fibrosis were observed. Lipid peroxidation and iron metabolism disorders were evident， as shown by significantly decreased SOD and GSH levels and significantly increased MDA and renal total iron levels （P<0.05， P<0.01）. Compared with the model group， all the above indices were significantly improved after DHGC intervention in a dose-dependent manner （P<0.05， P<0.01）. In vitro， compared with the blank group， HK-2 cell viability was significantly decreased in the model group. A concentration of 0.4 μmol·L-1 erastin was identified as the optimal induction dose， and high-dose DHGC-containing serum was identified as the optimal treatment condition. Compared with the model group， cell viability was significantly increased in all DHGC-containing serum groups （P<0.05， P<0.01）. Mechanistically， compared with the blank group， protein expression of SIRT3 and GPX4 was significantly decreased in both in vivo and in vitro model groups， while p53 and ac-p53 expression and p53 nuclear translocation were significantly increased （P<0.01）. Compared with the model group， these changes were significantly reversed after DHGC intervention （P<0.05， P<0.01）.ConclusionDHGC exerts a protective effect against adenine-induced CKD in mice and erastin-induced ferroptosis in HK-2 cells. The mechanism is associated with its anti-ferroptosis effect mediated via the SIRT3/p53 signaling pathway.Keywords：Dahuang Gancaotang;chronic kidney disease;ferroptosis;silent information regulator 3 （SIRT3）;deacetylation80|61|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Exploring Mechanism and Treatment of Senile Insomnia Based on Theory of Extreme Yang AI Introduction
Abstract：Senile insomnia is a common clinical disorder. Traditional Chinese medicine （TCM） primarily attributes the pathogenesis of insomnia to Yang failing to enter Yin aspect and disharmony between Yin and Yang. However， the discussion on insomnia caused by Yang Qi deficiency in elderly patients remains insufficient. According to the theory of extreme Yang in the Huang Di Nei Jing， this paper systematically elucidates the central role of Yang Qi in maintaining mental tranquility and regulating the sleep-wake cycle. It posits that the natural decline of Yang Qi with aging leads to Yang failing to enter Yin aspect or deficient Yang floating upward， which constitutes a key pathogenesis of senile insomnia. From a modern medical perspective， mitochondrial energy metabolism dysfunction is identified as a crucial biological basis. Mitochondrial functional declines result in insufficient adenosine triphosphate （ATP） production and reactive oxygen species （ROS） accumulation， which disrupts the synthesis of sleep-related neurotransmitters and the expression of circadian clock genes， ultimately leading to sleep disturbances. Furthermore， this sutdy explores the intrinsic connection between Yang Qi deficiency and mitochondrial dysfunction， arguing for a high degree of correspondence in their functional and pathological manifestations. Accordingly， the therapeutic principle of warming and tonifying Yang Qi， nourishing the heart and tranquilizing the mild is proposed. This approach employs Yang-warming formulas and acupuncture to regulate the mitochondrial function through multiple targets. Specific mechanisms include enhancing the activity of respiratory chain complexes， activating the mitochondrial autophagy， and mitigating oxidative stress， thereby restoring energy metabolic homeostasis and improving sleep in the elderly. This study provides a new theoretical foundation and a therapeutic strategy for integrating TCM and Western medicine in preventing and treating senile insomnia.Keywords：Huang Di Nei Jing;extreme Yang;mitochondrial dysfunction;senile insomnia76|47|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06- Abstract：ObjectiveTo investigate the mechanism by which Anmei Dan （AMD） regulates recombinant sirtuin 3/nuclear factor erythroid 2-related factor 2（SIRT3/Nrf2） signaling to ameliorate mitochondrial oxidative stress and improve the cognitive function in aged sleep-deprived mice.MethodsSixty aged C57 mice were randomly assigned to a control group， a model group， a melatonin （1.3 mg·kg-1·d-1） group， and high-， medium-， and low-dose （26.26， 13.13， 6.565 g·kg-1·d-1， respectively） AMD groups， with ten mice per group. Continuous sleep deprivation was administered for 4 weeks via a custom-built sleep deprivation chamber. The cognitive function of mice was assessed via the Morris water maze test. Hematoxylin-eosin （HE） staining was performed to observe morphological alterations in pyramidal neurons. Biochemical assays were carried out to measure the hippocampal and serum levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione peroxidase （GSH-Px）， catalase （CAT）， and total antioxidant capacity （T-AOC）. Transmission electron microscopy was adopted to examine mitochondrial pathological alterations in the hippocampus. Immunohistochemical assay was conducted to examine the expression of nuclear factor E2-related factor 2 （Nrf2）， sirtuin 3 （SIRT3）， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， mitochondrial transcription factor A （TFAM）， and brain-derived neurotrophic factor （BDNF） in the mouse hippocampus. The protein levels of Nrf2， SIRT3， heme oxygenase-1 （HO-1）， and NAD（P）H：quinone oxidoreductase 1 （NQO1） in mouse hippocampal tissue were determined by Western blot. Immunofluorescence double labeling was employed to determine the protein levels of SIRT3/Nrf2 in mouse hippocampal tissue.ResultsCompared with the control group， the model group exhibited prolonged latency to navigate， increased total swimming distance， reduced number of platform crossings， and shortened time spent in the target quadrant （P<0.05， P<0.01）， disorganized morphology and arrangement of hippocampal neurons， with increased damaged mitochondria， mitochondrial swelling， reduced cristae， and vacuolization， declined levels of SOD， GSH-Px， CAT， and T-AOC and elevated levels of MDA in the hippocampus and serum （P<0.01）， and downregulated protein levels of SIRT3， Nrf2， PGC-1α， TFAM， BDNF， HO-1， and NQO1 （P<0.01）. Compared with the model group， the melatonin group and AMD groups exhibited shortened spatial navigation latency， reduced total swimming distance， increased number of platform crossings， and prolonged activity time in the target quadrant （P<0.05， P<0.01）， reduced neuronal damage and mitochondrial damage in the hippocampal tissue， declined level of MDA and elevated levels of SOD， GSH-Px， CAT， and T-AOC in the hippocampus and serum （P<0.05， P<0.01）， and upregulated protein levels of SIRT3， Nrf2， PGC-1α， TFAM， BDNF， HO-1， and NQO1 in the hippocampus （P<0.05， P<0.01）.ConclusionAMD may improve the learning and memory in aged sleep-deprived mice by mediating mitochondrial oxidative damage through the SIRT3/Nrf2 signaling pathway.Keywords：Anmei Dan;aged sleep deprivation;cognitive function;mitochondrial oxidative stress;recombinant sirtuin 3/nuclear factor erythroid 2-related factor 2（SIRT3/Nrf2） signaling pathway55|50|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06
- Abstract：ObjectiveTo investigate whether Anmei Dan （AMD） improves cognitive function and alleviates circadian rhythm disorders in an aged mouse model of sleep deprivation by inhibiting the erythropoietin-producing hepatocellular receptor A4 （EphA4）/Eph receptor-interacting protein A3 （EphrinA3） signaling pathway and its downstream Ras homolog family member A （RhoA）/Rho-associated coiled-coil containing protein kinase （ROCK） signaling， and to analyze its multi-target regulatory characteristics.MethodsAn aged C57 mouse model of sleep deprivation was established by the modified multiple platform water environment method. The mice were randomized into blank， model， rhynchophylline （Rhy， antagonist， 50 mg·kg-1·d-1）， and antagonist plus AMD （26.26 g·kg-1·d-1） groups. Spontaneous activity was assessed by the open field test， and circadian rhythm activity was monitored. Hematoxylin-eosin （HE） staining and Nissl staining were conducted to observe neuronal morphology in the hippocampal CA1/CA3 regions. Western blot and immunofluorescence assay were employed to determine the protein levels of EphA4， EphrinA3， Neuronal Nuclei Antigen （NEUN）， glial fibrillary acidic protein （GFAP）， phosphorylated （p）-EphA4， RhoA， Rho-associated coiled-coil containing protein kinase 1 （ROCK1）， Rho-associated coiled-coil containing protein kinase 2 （ROCK2）， brain-derived neurotrophic factor （BDNF）， synaptophysin （SYN）， postsynaptic density protein 95 （PSD95）， and growth-associated protein 43 （GAP43）. The mRNA levels of EphA4 and EphrinA3 were determined by real-time PCR.ResultsCompared with the blank group， the model group showed decreased spontaneous activity （P<0.01）， circadian rhythm disruption （P<0.01）， hippocampal neuron disarrangement and reduced Nissl bodies， upregulated protein levels of EphA4， EphrinA3， NEUN， p-EphA4， RhoA， ROCK1， ROCK2， and GFAP （P<0.01）， and downregulated protein levels of NEUN， BDNF， SYN， PSD95， and GAP43 （P<0.01）. Compared with the model group， both the antagonist group and the antagonist plus AMD group showed recovery in the above indicators （P<0.05， P<0.01）， with the combination group outperforming the antagonist group in behavioral， pathological， and molecular expression aspects （P<0.05， P<0.01）.ConclusionAMD can alleviate cognitive and rhythm disorders caused by sleep deprivation by inhibiting the EphA4/EphrinA3 signaling pathway and its downstream RhoA/ROCK signaling， and upregulating the expression of synapse-related proteins such as BDNF. Its combination with an EphA4 antagonist exhibits a synergistic effect， which suggests that the mechanism involves multi-link synergistic intervention.Keywords：Anmei Dan （AMD）;sleep deprivation;erythropoietin-producing hepatocellular receptor A4 （EphA4）/Eph receptor-interacting protein A3 （EphrinA3） signaling pathway;cognitive function;synapse48|39|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06
Anmei Dan Regulates Hippocampal Inflammation via CX3CL1/CX3CR1 Signaling Pathway to Improve Learning and Memory in Aged Sleep-deprived Mice AI Introduction
Abstract：ObjectiveTo investigate the effects of Anmei Dan （AMD） on the expression of proteins in the C-X3-C motif chemokine ligand 1 （CX3CL1）/C-X3-C chemokine receptor 1 （CX3CR1） signaling pathway， hippocampal inflammation， and learning and memory in an aged sleep-deprived model.MethodsSixty aged C57 mice were randomly assigned into a control group， a model group， a melatonin group （1.3 mg·kg-1·d-1）， and high-， medium-， and low-dose AMD groups （26.26， 13.13， 6.565 g·kg-1·d-1， respectively）， with 10 mice per group. Continuous sleep deprivation was administered for 4 weeks through a custom-built sleep deprivation chamber. The cognitive function of mice was assessed via the Y-maze test. Histomorphological alterations in pyramidal cells of the hippocampal CA1 and DG regions were examined by hematoxylin-eosin （HE） and Nissl staining. Synaptic morphology in the hippocampus was visualized with Golgi staining. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of inflammatory cytokines interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） in the hippocampal tissue as well as the level of interleukin-10 （IL-10） in the prefrontal cortex. Real-time PCR was performed to detect markers of M1-type ［cluster of differentiation （CD） 86 and inducible nitric oxide synthase （iNOS）］ and M2-type ［CD206 and arginase 1 （Arg1）］ macrophages. Western blot was employed to quantify the protein levels of CX3CL1， CX3CR1， phosphorylated nuclear factor κB p65 subunit （p-NF-κB p65）， and phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK） in the hippocampus. Immunofluorescence double staining was performed to co-label CX3CR1 with ionized calcium-binding adapter molecule 1 （Iba-1） for observation of the co-localization of target proteins with microglia.ResultsCompared with the control group， the model group exhibited disrupted daily activity patterns with reduced spontaneous alternation rates （P<0.01）， disorganized morphology and arrangement of hippocampal neurons， accompanied by reduced numbers of Nissl bodies and dendritic spines （P<0.01）， upregulated protein levels of IL-6， IL-10， IL-1β， TNF-α， CX3CL1， CX3CR1， p-NF-κB p65， p-p38 MAPK， and Iba-1 and mRNA levels of CD86 and iNOS （P<0.01）， and downregulated mRNA levels of CD206 and Arg1 （P<0.05，P<0.01）. Compared with the model group， the melatonin group and medium- and high-dose AMD groups showed increased spontaneous alternation rates （P<0.01）， improved neuronal morphology， number， and spine density in the hippocampal CA1 and DG regions （P<0.01）， declined levels of IL-6， IL-10， IL-1β， and TNF-α （P<0.05， P<0.01）， downregulated protein levels of CX3CL1， CX3CR1， p-NF-κB p65， p-p38 MAPK， and Iba-1 and mRNA levels of CD86 and iNOS， and upregulated mRNA levels of CD206 and Arg1 （P<0.01）.ConclusionAMD may improve the learning and memory in aged sleep-deprived mice by mediating neuroinflammation through the CX3CL1/CX3CR1 signaling pathway.Keywords：Anmei Dan;aged sleep deprivation;neuroinflammation;learning and memory;C-X3-C motif chemokine ligand 1 （CX3CL1）/C-X3-C motif chemokine receptor 1 （CX3CR1） signaling pathway65|39|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Clinical Efficacy and Mechanism of Anmei Dan in Treating Insomnia with Amnesia Based on Principle of Treating Different Diseases with Same Method： A Review Enhanced Publication AI Introduction
Abstract：In modern society， the comorbidity of insomnia with amnesia has shown a significantly increasing incidence and become increasingly severe， emerging as a public health issue that endangers people's physical and mental health and quality of life. Anmei Dan （AMD）， originally recorded in the Shishi Milu by CHEN Shiduo in the Qing Dynasty， possesses profound theoretical foundations and distinct clinical advantages in ameliorating insomnia with amnesia. Basic research has unequivocally confirmed its definite therapeutic effects on insomnia with amnesia and revealed partial mechanisms. AMD is therefore a veritable classic prescription embodying the principle of treating different diseases with the same method for insomnia and amnesia. However， few researchers have reviewed the related research progress. This article systematically summarized the theoretical connotations of traditional Chinese medicine in treating insomnia with amnesia， delineated the multi-component material basis of AMD in ameliorating insomnia with amnesia （including various chemical components such as ginsenosides， jujubosides， and salvianolic acids）， and evaluate its multi-dimensional clinical efficacy （e.g.， prolonging total sleep time， improving sleep efficiency， and enhancing memory）. Moreover， it systematically summarizes the multi-pathway mechanisms of action. The results indicate that AMD has a clear material basis， definite clinical efficacy， and a favorable safety profile in ameliorating insomnia and amnesia. AMD may exert the therapeutic effect by regulating sleep-wake rhythms， enhancing synaptic plasticity， inhibiting neuroimmune inflammation， and modulating autophagy， oxidative stress， and energy metabolism. In conclusion， AMD exerts synergistic effects through multi-component， multi-dimensional， and multi-pathway approaches， serving as an important prescription for enriching and developing the theory of treating different diseases with the same method for insomnia with amnesia.Keywords：Anmei Dan;treating different diseases with the same method;insomnia;amnesia;mechanism of action58|40|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Effect of Aerobic Exercise Combined with Anmeidan on Learning Memory and Synaptic Plasticity in Rats with Sleep Deprivation Based on BDNF/TrkB/CREB Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveThis paper aims to study the effects of four weeks of aerobic exercise combined with Anmeidan on the synaptic plasticity marker protein and synaptic ultrastructure of the hippocampus in the model rats with sleep deprivation， thereby investigating the possible mechanism of its action to improve the learning memory of rats with sleep deprivation.Methods50 Sprague-Dawley （SD） rats were randomly divided into blank control group （group C）， sleep deprivation group （group M）， aerobic exercise + sleep deprivation group （group MEX）， Anmeidan + sleep deprivation group （group MA， 18.18 g∙kg-1∙d-1）， and aerobic exercise + Anmeidan + sleep deprivation group （group MEXA， 18.18 g∙kg-1∙d-1）. Anmeidan was administered by gavage in the MA group for four weeks. Aerobic exercise was performed in the MEX group for four weeks. Anmeidan was administered by gavage in the MEXA group in combination with aerobic exercise for four weeks， and sleep deprivation was performed for 72 h by using the multi-platform water environment method. At the end of sleep deprivation， Morris water maze was used to assess the learning and memory ability of rats in each group， and hematoxylin-eosin （HE） staining was used to observe the morphological changes of rats' hippocampal neurons. A transmission electron microscope was used to observe the synaptic ultrastructure of rats' hippocampus. The expression levels of brain-derived neurotrophic factor （BDNF）， tyrosine kinase receptor B （TrkB）， cAMP-response element binding protein （CREB）， postsynaptic density-95 （PSD-95）， and synaptophysin （SYN） were detected by Western blot， and the real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the relative mRNA expression levels of BDNF， TrkB， and CREB in the rats' hippocampus.ResultsCompared with those in group C， rats in group M had significantly longer latency and total swimming distance on the platform （P<0.01） and a significantly reduced number of traversals across the platform as well as the residence time in the target quadrant （P<0.01）. Part of the hippocampal neurons damaged， with a reduced number， disorganized arrangement， fuzzy synaptic gaps， thinning of post-synaptic dense material， and uneven density of synaptic vesicles. The protein expression levels and relative mRNA expression levels of BDNF， TrkB， and CREB were significantly reduced （P<0.01）， and the protein expression levels of PSD-95 and SYN were significantly reduced （P<0.01）. Compared with those in group M， rats in MA， MEX， and MEXA groups showed a decrease in latency to platform and total distance swum， an increase in the number of traversals across the platform and residence time in the target quadrant （P<0.05， P<0.01）， a reduction in hippocampal neuronal damage， a better arrangement， a more intact synaptic structure， a thickening of post-synaptic dense material， a uniform density of synaptic vesicles， and an increase in the protein expression levels and mRNA expression levels of BDNF， TrkB， and CREB （P<0.05， P<0.01）. The protein expressions of PSD-95 and SYN rose （P<0.05， P<0.01）.ConclusionAerobic exercise combined with Anmeidan can improve learning memory in rats with sleep deprivation， and its mechanism of action may be related to the modulation of the BDNF/TrkB/CERB signalling pathway， up-regulation of the expression of PSD-95 and SYN， and improvement of synaptic structural damage. The combination of interventions is superior to single exercise or drugs.Keywords：Anmeidan;Aerobic exercise;sleep deprivation;learning memory;synaptic plasticity;brain-derived neurotrophic factor （BDNF）/tyrosine kinase receptor B （TrkB）/ cAMP-response element binding protein （CERB）65|60|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Mechanisms of Tongmai Yangxin Pills and Tongxinluo Capsules in Treating Myocardial No-reflow Based on Treating Same Disease with Different Methods Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the mechanisms of Tongmai Yangxin pills （TMYX） and Tongxinluo capsules （TXL） in treating no-reflow （NR） after myocardial ischemia and reperfusion following the concept of treating the same disease with different methods， based on integrative pharmacology and experimental validation.MethodsEighty 8-week-old SPF-grade SD rats were randomly assigned into four groups （n=20）： sham operation， NR， TMYX （4 g·kg-1）， and TXL （2 mg·kg-1）. A rat model of myocardial ischemia-reperfusion no-reflow was established by in-situ ligation of the left anterior descending coronary artery. Gastric gavage was first performed 4 h after the operation， and samples were collected on day 7. Thioflavin S staining was used to observe the NR area in rat myocardium. Echocardiography was performed to examine the cardiac function. Hematoxylin-eosin （HE） staining was conducted to observe the pathological changes of the myocardial tissue. An automatic biochemical analyzer was adopted to measure myocardial enzyme activity. Then， integrated pharmacology was applied for Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis. Finally， Western blot was employed to quantify the protein levels of key targets in the myocardial tissue， including soluble guanylyl cyclase （sGC）， cyclic guanosine monophosphate （cGMP）/dependent protein kinase （PKG）， phosphorylated phosphatidylinositol 3-kinase （p-PI3K）， phosphorylated protein kinase B （p-Akt）， and hypoxia-inducible factor-1α （HIF-1α）.ResultsCompared with the sham operation group， the NR group showed increased NR area of myocardium， decreased left ventricular ejection fraction （EF）， left ventricular fractional shortening （FS）， left ventricular outflow tract peak velocity （LVOT Peak）， and left ventricular stroke volume （LVSV） （P<0.01）， fractured and disordered myocardial fibers as well as inflammatory cell infiltration in the myocardial tissue， enhanced activities of creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， and lactate dehydrogenase （LDH） in the myocardial tissue （P<0.01）， and downregulated protein levels of sGC， PKG， phosphorylated （p）-PI3K （Tyr458）， and p-Akt （Tyr315） in the myocardial tissue （P<0.05， P<0.01）. The expression level of HIF-1α protein showed a downward trend. Compared with the NR group， the TMYX group and TXL group exhibited a decreasing trend in myocardial NR area， EF， FS， and LVOT Peak significantly increased （P<0.05， P<0.01）， LVSV showed an upward trend， ameliorated myocardial pathological morphology and inflammatory infiltration， reductions in CK， CK-MB， and LDH activities （P<0.05， P<0.01）， and upregulated protein levels of sGC， PKG， p-PI3K （Tyr458） in myocardial tissue （P<0.05， P<0.01）， the protein expressions of p-Akt （Tyr315） and HIF-1α showed an upward trend. A comparison of the therapeutic effects between the two compound prescriptions showed that TMYX tended to exert a better effect in restoring cardiac function and protecting cardiac structure in NR rats， whereas TXL was more effective in reducing myocardial NR area and lowering myocardial enzyme activities in NR rats. Integrative pharmacology analysis combined with experimental verification demonstrated that both TMYX and TXL could alleviate NR through the following mechanisms： activating the cyclic cGMP/PKG signaling pathway to regulate vascular tone， activating the PI3K/Akt signaling pathway to dilate blood vessels， and activating the HIF-1 signaling pathway to inhibit oxidative stress. However， TMYX had an advantage in activating the cGMP/PKG pathway， while TXL was superior in activating the PI3K/Akt pathway. The two compound prescriptions exerted comparable effects on the HIF-1 signaling pathway， which might serve as their common therapeutic pathway.ConclusionBoth TMYX and TXL could alleviate NR damage. TMYX exerts its protective effect against NR mainly by activating the cGMP/PKG signaling pathway， while TXL exerts its effect mainly through the PI3K/Akt pathway. The HIF-1α signaling pathway may be a common pathway for the two compound prescriptions to exert their protective effects against NR. This study reveals the similarities and differences between TMYX and TXL in the treatment effect and mechanism for NR， providing an experimental basis and a theoretical basis for better clinical application of the two compound prescriptions.Keywords：Tongmai Yangxin pills;Tongxinluo;treating the same disease with different methods;no-reflow after myocardial ischemia and reperfusion;integrative pharmacology65|32|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Mechanism of Chidamide Combined with Compound Kushen Injection on Breast Cancer Cells Based on Transcriptomics Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the synergistic inhibitory effect of chidamide （CHI） combined with compound Kushen injection （CKI） on breast cancer MCF-7 cells and to elucidate the potential molecular mechanisms based on transcriptomics analysis.MethodsCell proliferation was detected by the methyl thiazolyl tetrazolium （MTT） assay， and the "one belt and one line" method was adopted to screen the optimal mass concentration for synergistic effect. According to the combination index （CI） values， cells were allocated into the blank， CHI （1.6 mg·L-1）， CKI （0.4 g·L-1）， and CHI+CKI （1.6 mg·L-1+0.4 g·L-1） groups. Transwell assay was employed to examine cell migration， and flow cytometry to measure cell cycle distribution and apoptosis rate. Transcriptome sequencing （RNA-seq） and weighted gene co-expression network analysis （WGCNA） were performed to screen the key modules highly correlated with the cell inhibition rate. Candidate genes were identified by intersecting module genes with differentially expressed genes （DEGs）， followed by functional enrichment analysis. Western blot was employed to quantify the protein levels of histone deacetylase 1 （HDAC1）， protein kinase A （PKA）， cyclin-dependent kinase inhibitor 1 （p21）， cAMP response element-binding protein （CREB） and its phosphorylated form （p-CREB）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in cells of each group.ResultsCompared with the blank group， both CHI and CKI monotherapies inhibited the proliferation of MCF-7 cells in a mass concentration-dependent manner. Compared with the blank and monotherapy groups， CHI+CKI inhibited cell migration， increased the proportion of cells arrested in the G0/G1 phase， and elevated the apoptosis rate （P<0.01）. WGCNA identified the MEred module strongly correlated with the inhibition rate （r=0.90， P<0.01）， yielding 97 candidate genes upon intersection with DEGs. Kyoto Encyclopedia of Genes and Genomes （KEGG） analysis indicated significant enrichment of the cAMP signaling pathway. Western blot results showed that compared with the blank group， all treatment groups down-regulated the expression of HDAC1， up-regulated the expression of PKA and p21， and increased the p-CREB/CREB and Bax/Bcl-2 ratios （P<0.01）. Compared with the monotherapy groups， CHI+CKI further up-regulated the PKA and p21 expression and increased the p-CREB/CREB and Bax/Bcl-2 ratios （P<0.01）.ConclusionThe combination of CHI and CKI exerts a significant synergistic anti-tumor effect. CHI exerts epigenetic regulation by inhibiting HDAC1， which， in combination with CKI， may further contribute to the activation of the cAMP/PKA/CREB signaling pathway， leading to up-regulation of p21 expression and the Bax/Bcl-2 ratio， thereby promoting cell cycle arrest and apoptosis.Keywords：chidamide;compound Kushen injection;breast cancer;synergism;transcriptomics;cyclic adenosine monophosphate （cAMP） signaling pathway86|70|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Mechanism of Feiyanning Formula in Suppressing Invasion and Metastasis of Lung Cancer Cells via Modulating Exosomal miR-328 and STAT3/c-Fos/NFATc1 Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the molecular mechanism by which Feiyanning formula（FYN） regulated exosomal miR-328 to suppress the invasion and metastasis of lung cancer.MethodsIn vitro models using low-metastatic 95C and high-metastatic 95D lung cancer cell lines， along with isolated exosomes， were established. Initially， 95C and 95D cells were cultured， and exosomes were isolated from their supernatants. The exosomes were identified using transmission electron microscopy （TEM）， nanoparticle tracking analysis （NTA）， and Western blot. Exosome uptake assays confirmed that both 95C and 95D cells could internalize exosomes derived from lung cancer patients' plasma. Cell counting kit-8 （CCK-8） assays were performed to assess the inhibitory effects of FYN （0， 0.1， 0.2， 0.4， 0.8， 1.6， 3.2， 6.4 g·L-1） on 95C and 95D cell proliferation. Subsequent experiments were divided into three groups of control， low-dose FYN （1 g·L-1）， and high-dose FYN （2 g·L-1） groups. Wound-healing and Transwell assays were used to evaluate the inhibitory effects of FYN on the migration and invasion of 95C and 95D cells. Western blot was employed to detect the protein expression levels of Janus kinase 2 （JAK2）， signal transducer and activator of transcription 3 （STAT3）， cellular oncogene Fos （c-Fos）， and nuclear factor of activated T cells 1 （NFATc1）. The mRNA expression of miR-328 was measured by Real-time quantitative polymerase chain reaction （Real-time PCR）.ResultsLung cancer plasma-derived exosomes （EXO） enhanced the migration， invasion， and miR-328 expression levels in 95C and 95D cells （P<0.05， P<0.01）. FYN inhibited the proliferation， invasion， and metastasis of 95C and 95D cells in a dose-dependent manner （P<0.01）， with more pronounced effects on 95C cells. Additionally， FYN downregulated exosomal miR-328 expression and suppressed the protein levels of JAK2， STAT3， and its downstream target genes c-Fos and NFATc1 （P<0.01）.ConclusionFYN may inhibit lung cancer metastasis by downregulating exosomal miR-328 expression， potentially through the STAT3/c-Fos/NFATc1 signaling pathway. Further studies are warranted to elucidate its detailed mechanisms and facilitate clinical application， providing insights into traditional Chinese medicine-based strategies for lung cancer treatment.Keywords：Feiyanning formula;exosome;miR-328;lung cancer;invasion and metastasis53|58|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Renal Protective Effect of Tongxinluo Submicron Powder on Mice with Diabetic Kidney Disease Based on PANoptosis AI Introduction
Abstract：ObjectiveTo investigate the role and underlying mechanisms of Tongxinluo submicron powder in regulating renal PANoptosis， alleviating pathological injury in diabetic kidney disease （DKD）， reducing urinary albumin excretion， and improving renal function in DKD mice.MethodsSix 6-week-old male C57BL/Ks mice were assigned into the normal group. Eighteen 6-week-old male BKS-db；Nos3KO mice were randomly divided into three groups： model group， Tongxinluo group （0.75 g·kg-1·d-1）， and dapagliflozin group （0.001 g·kg-1·d-1）， and were administered by gavage for 12 consecutive weeks. General conditions of the mice were observed. At weeks 0， 4， 8， and 12 after administration， body weight， fasting blood glucose （FBG）， urine albumin-to-creatinine ratio （UACR）， and urinary albumin excretion rate （AER） were measured. After treatment， mice were anesthetized for sample collection. Blood was obtained by orbital enucleation and centrifuged to collect supernatant. Serum creatinine （SCr）， urea （UREA）， β2-microglobulin （β2-MG）， retinol-binding protein （RBP）， and serum cystatin C （CysC） were measured. Renal histopathological changes were evaluated using hematoxylin-eosin （HE） staining， periodic acid-Schiff （PAS） staining， and Masson's trichrome staining. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of inflammatory cytokines， including interleukin-1β （IL-1β）， interleukin-18 （IL-18）， and tumor necrosis factor-α （TNF-α）. Serum levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， and glutathione peroxidase （GSH-Px） were also measured. Western blot analysis was performed to quantify the expression of key PANoptosis-related proteins in renal tissue， including Z-DNA-binding protein 1 （ZBP1）， Caspase-1， cleaved Caspase-1， gasdermin D （GSDMD） and its N-terminal fragment （GSDMD-N）， Caspase-8， cleaved Caspase-8， Caspase-3， cleaved Caspase-3， mixed lineage kinase domain-like protein （MLKL）， and phosphorylated MLKL （p-MLKL）.ResultsCompared with the normal group， the model group showed significant obesity and continuously increased blood glucose levels （P<0.05）. Renal function indicators （UREA， β2-MG， CysC） were significantly increased （P<0.05）， and urinary albumin excretion indicators （UACR， AER） were markedly elevated （P<0.05）. Renal histopathology showed enlarged glomeruli， diffuse thickening of the basement membrane， and significant expansion of the mesangial matrix. Masson staining revealed extensive blue collagen fiber deposition， suggesting glomerulosclerosis and interstitial fibrosis. Meanwhile， serum levels of inflammatory cytokines （IL-1β， IL-18， and TNF-α） were significantly increased （P<0.05）. SOD and GSH-Px levels were decreased， while MDA levels were increased （P<0.05）. The expression of key PANoptosis-related proteins （ZBP1， cleaved Caspase-1， GSDMD， GSDMD-N， cleaved Caspase-8， Caspase-3， cleaved Caspase-3， and p-MLKL） in renal tissue was significantly upregulated （P<0.05）. After intervention， compared with the model group， renal function indicators （UREA， β2-MG， CysC） and urinary albumin excretion indicators （UACR， AER） in the Tongxinluo group were significantly decreased （P<0.05）， and all were superior to those in the dapagliflozin group （P<0.05）. Renal pathological injury was markedly alleviated， with reduced mesangial proliferation and collagen fiber deposition. In addition， serum levels of IL-1β， IL-18， and TNF-α were significantly decreased （P<0.05）. SOD and GSH-Px levels were increased， while MDA levels were decreased （P<0.05）. Western blot results showed that the expression of key PANoptosis-related proteins （ZBP1， cleaved Caspase-1， GSDMD， GSDMD-N， cleaved Caspase-8， Caspase-3， cleaved Caspase-3， and p-MLKL） in renal tissue was significantly downregulated （P<0.05）.ConclusionTongxinluo submicron powder can inhibit renal PANoptosis in DKD mice， alleviate renal inflammatory response and pathological injury， reduce urinary albumin excretion， and improve renal function.Keywords：diabetic kidney disease;BKS-db;Nos3KO mice;Tongxinluo submicron powder;PANoptosis;renal protection70|59|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Sanjie Quban Prescription Affects Proliferation， Apoptosis， Migration， and Invasion of Human Keloid Fibroblasts via AhR/CYP1A1 Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the effects of Sanjie Quban prescription （SJQB）-containing serum on the proliferation， apoptosis， migration， and invasion of human keloid fibroblasts （KFs） and to elucidate its underlying mechanism， with a focus on the aryl hydrocarbon receptor （AhR）/cytochrome P450 family 1 subfamily A member 1 （CYP1A1） signaling pathway.MethodsPrimary human KFs were cultured in vitro and assigned to the following groups： control （KFs+blank serum）， asiaticoside （KFs+asiaticoside-containing serum）， SJQB （KFs+SJQB-containing serum）， AhR agonist （KFs+β-naphthoflavone）， AhR inhibitor （KFs+CH223191）， and AhR inhibitor+SJQB （KFs+CH223191+SJQB-containing serum）. The optimal intervention concentrations were determined through the cell counting kit-8 （CCK-8） assay. Cell proliferation， apoptosis， migration， and invasion were evaluated by the EdU assay， flow cytometry， wound healing assay， and Transwell assay， respectively. The expression of transforming growth factor-β1 （TGF-β1） and α-smooth muscle actin （α-SMA） was visualized by immunofluorescence. The mRNA and protein levels of AhR， CYP1A1， TGF-β1， and α-SMA were measured by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively.ResultsCompared with the control group， the SJQB， asiaticoside， and AhR agonist groups demonstrated inhibited cell proliferation， migration， and invasion， along with an increased apoptosis rate （P<0.01）. The AhR inhibitor group showed enhanced proliferation， migration， and invasion together with a reduced apoptosis rate in comparison with the AhR agonist group （P<0.01）. The AhR inhibitor+SJQB group exhibited increased proliferation， migration， and invasion as well as decreased apoptosis compared with the SJQB group （P<0.05， P<0.01）. At the molecular level， compared with the control group， the SJQB， asiaticoside， and AhR agonist groups presented upregulated protein and mRNA levels of AhR and CYP1A1 （P<0.05， P<0.01）， while the SJQB and AhR agonist groups showed downregulated TGF-β1 and α-SMA expression at both protein and mRNA levels （P<0.05， P<0.01）， and the asiaticoside group displayed decreased protein level of TGF-β1 and mRNA level of α-SMA （P<0.05， P<0.01）. Compared with both the AhR agonist and control groups， the AhR inhibitor group exhibited decreased AhR and CYP1A1 expression but increased TGF-β1 and α-SMA expression at protein and mRNA levels （P<0.01）. In comparison with the SJQB group， the AhR inhibitor+SJQB group demonstrated reduced AhR and CYP1A1 expression （P<0.01） and elevated TGF-β1 and α-SMA expression （P<0.05， P<0.01） at both protein and mRNA levels.ConclusionSJQB may activate the AhR/CYP1A1 signaling pathway to downregulate TGF-β1 and α-SMA expression， thereby suppressing the proliferation， migration， and invasion and inducing the apoptosis of KFs.Keywords：Sanjie Quban prescription;aryl hydrocarbon receptor （AhR）/cytochrome P450 family 1 subfamily A member 1 （CYP1A1） signaling pathway;keloid;fibroblast60|32|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Expert Consensus on Treatment of Simple Obesity in Children with Chinese Herbal Medicine AI Introduction
Abstract：Childhood obesity is a chronic nutritional disorder caused by multiple factors that result in excessive total body fat and/or increased local fat content and abnormal fat distribution，sometimes accompanied by complications such as metabolic syndrome. The obesity caused by other factors excluding the secondary factors like genetics or metabolism is referred to as simple obesity. The incidence of childhood obesity in China is showing a trend toward younger ages and rapid growth，posing a serious threat to people's health and creating a heavy economic burden. Therefore，it is urgent to control and effectively intervene in childhood obesity. Traditional Chinese herbal medicine has long been a representative of internal treatment and shows effectiveness and advantages in the clinical treatment of childhood obesity. However，there is currently a lack of a comprehensive set of diagnostic and treatment standards，as well as evidence-based clinical practice. In order to improve clinical physicians' understanding of this disease and to promote the standardization and rationalization of herbal treatment，experts in clinical Chinese and Western medicine，nutrition，and methodology from across China were invited. On the basis of expert experience and current evidence，the Grading of Recommendations Assessment，Development，and Evaluation （GRADE） method was used to grade the evidence and recommendations. After two rounds of Delphi expert consultations，the guideline secretariat revised and refined the materials based on expert opinions. Ultimately，14 entries of expert consensus and recommendations were formulated，highlighting the advantages and characteristics of herbal treatment for childhood obesity，clarifying syndrome differentiation，medication，treatment cycles，and combination therapy plans for common clinical syndromes，thereby providing more treatment ideas in clinical practice and better leveraging therapeutic advantages.Keywords：childhood obesity;Chinese herbal medicine;diagnosis and treatment standards;expert consensus112|45|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06- Abstract：ObjectiveToll-like receptor 4 （TLR4）， a receptor for pathogen-associated molecular patterns of innate immunity， is associated with neurodegenerative diseases. Interleukin （IL）-6， IL-1β， and tumor necrosis factor-α （TNF-α） as common pro-inflammatory cytokines and high-sensitivity C-reactive protein （hs-CRP） are related to inflammatory responses. This study evaluated the clinical efficacy and possible mechanisms of therapeutic effects of Fengyintang on early and mid-stage PD with excessive heat generating wind by observing the effects of Fengyintang on the serum levels of TLR4， IL-6， IL-1β， TNF-α， and hs-CRP in the patients with PD.MethodsSixty-eight PD patients who met the inclusion criteria were randomly assigned into the control group and the observation group （n=34）. Both groups were treated with anti-PD Western medicine and the observation group was additionally treated with Fengyintang. Both groups were treated for 8 weeks. Before and after 8 weeks of treatment， the patients in the two groups were measured for their TCM symptom scores， International Movement Disorder Society Unified Parkinson's Disease Rating Scale （MDS-UPDRS） score， Parkinson's Disease Non-Motor Symptom Scale （NMSS） score， Patient Assessment of Constipation Symptom （PAC-SYM） score， Pittsburgh Sleep Quality Index （PSQI）， Hamilton Anxiety Scale （HAMA） score， Hamilton Depression Scale （HAMD） score， and changes in serum TLR4， IL-6， IL-1β， TNF-α， and hs-CRP levels.ResultsOne case in the control group was removed due to loss of visit， and a total of 67 PD patients （33 in the control group and 34 in the observation group） who met the criteria were included for analysis. After treatment， patients in the observation group showed decreases in scores of TCM symptoms， MDS-UPDRS， NMSS， PAC-SYM， PSQI， HAMA， and HAMD （P<0.05， P<0.01）. Moreover， the observation group had lower scores of TCM symptoms， MDS-UPDRS， NMSS， PAC-SYM， PSQI， HAMA， and HAMD than the control group （P<0.05， P<0.01）. The observation group showed higher efficacy in terms of TCM symptoms and MDS-UPDRS score than the control group （Z=-0.57， P<0.05）. The overall response rate was higher in the observation group than in the control group （Z=-0.62， P<0.05， P<0.01）. The serum TLR4， TNF-α， IL-1β， IL-6， and hs-CRP levels of the observation group were lower than those of the control group （P<0.05， P<0.01）.ConclusionFengyintang combined with Western medicine can safely and effectively alleviate the clinical symptoms， reduce the levels of inflammatory factors， improve the quality of life， and delay the disease progression of PD patients by inhibiting peripheral TLR4 expression and thus suppressing the downstream inflammatory response.Keywords：Fengyintang;Parkinson's disease;neuroinflammation;inflammatory factors;non-motor symptoms78|80|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06
A Randomized Controlled Trial on Regulation of LncRNA EBLN3P/miR-369-3p/NFIX-JAK/STAT Signaling Pathway by Huangqin Qingre Chubi Capsules to Restore Clinical and Laboratory Indicators in Patients with Rheumatoid Arthritis Enhanced Publication AI Introduction
Abstract：ObjectiveTo evaluate the clinical efficacy of Huangqin Qingre Chubi capsules （HQC） in patients with rheumatoid arthritis （RA） and the syndrome of dampness-heat obstruction and investigate the mechanism by which HQC restore clinical and laboratory parameters in RA patients through regulation of the long non-coding RNA （LncRNA） endogenous Bornavirus-like nucleoprotein 3 pseudogene （EBLN3P）/miR-369-3p/nuclear factor I X（NFIX）-Janus kinase（JAK）/signal transducer and activator of transcription （STAT） signaling pathway，thereby providing new experimental evidence and potential therapeutic targets for the traditional Chinese medicine （TCM） treatment of RA.MethodsA randomized controlled trial design was adopted，with 100 RA patients meeting the criteria assigned into an observation group （n=50） and a control group （n=50）. In addition，50 healthy controls were enrolled. The control group received leflunomide plus meloxicam，while the observation group additionally received HQC. Efficacy was assessed after 4 weeks of treatment. Observation indicators including Western medicine indicators （DAS28，CPRI-RA，SF-36，VAS，PGA，PhGA，and SAS/SDS），TCM syndrome scores （TCMSS-RADHP，TCMSS-RASDP），and laboratory indicators （ESR，CRP，RF，anti-CCP antibody，VEGF，bFGF，MMP-2/9，p-JAK2/STAT3，and LncRNA EBLN3P/miR-369-3p/NFIX expression） were measured to comprehensively explore the therapeutic mechanism of HQC.ResultsThe study included 45 healthy controls （34 males and 11 females） and 87 RA patients （22 males and 65 females）. The median age，median disease duration，and median BMI of patients were 56 years old，10 years，and 21.51 kg·m-2，respectively. Compared with healthy controls，the RA group exhibited a typical state of immune-inflammatory activation as manifested by elevated levels of ESR，anti-CCP antibodies，CRP，and RF （P<0.01），raised clinical symptom scores （DAS28，VAS，PGA，PhGA，CPRI-RA，and TCM symptoms） （P<0.05，P<0.01），and reduced SF-36 domain scores （P<0.01）. Molecular detection revealed abnormal expression of LncRNA EBLN3P and miR-369-3p，upregulated expression of key proteins in the JAK/STAT pathway （JAK2/p-JAK2 and STAT3/p-STAT3） and angiogenesis markers （VEGF，bFGF，and MMP-2/9），and downregulated expression of NFIX （P<0.05，P<0.01） in the RA group. Spearman correlation analysis further demonstrated associations of key molecules in the LncRNA EBLN3P/miR-369-3p/NFIX-JAK/STAT pathway with immune-inflammatory markers and clinical symptom scores （P<0.05，P<0.01）. Regarding treatment response，both groups showed reductions in ESR，anti-CCP，CRP，and RF levels compared with baseline （P<0.01） and restored scores of DAS28，CPRI-RA，VAS，PGA，PhGA，TCM symptoms，SAS，SDS，and all SF-36 domains （P<0.01）. The observation group outperformed the control group in restoring the scores of SAS，SDS，PGA，TCMSS-SDP，and SF-36 domains （PF，BP，GH，VT，and SF） （P<0.05）. Real-time PCR analysis revealed that post-treatment expression levels of LncRNA EBLN3P，miR-369-3p，NFIX，JAK2，p-JAK2，STAT3，p-STAT3，VEGF，bFGF，MMP-2，and MMP-9 were recovered compared with pre-treatment levels （P<0.01）. Notably，the observation group demonstrated superior regulatory effects on p-JAK2，STAT3，p-STAT3，and MMP-9 compared with the control group （P<0.05）. Apriori association rule analysis revealed that HQC treatment was significantly correlated with reduced TCMSS-RADHP，ESR，SF，DAS28，SAS，and SDS scores，as well as increased VT，GH，and RP scores （confidence >80%，support >50%）. Regarding safety，two patients in the observation group experienced mild gastrointestinal discomfort，and one patient in the control group developed a rash. All the symptoms resolved after symptomatic treatment.ConclusionHQC target and regulate the LncRNA EBLN3P/miR-369-3p/NFIX-JAK/STAT axis to inhibit angiogenesis and inflammatory responses，reduce immune inflammatory markers，alleviate clinical symptoms，and improve the quality of life in RA patients，exerting synergistic effects on symptoms and quality of life.Keywords：Huangqin Qingre Chubi capsules;rheumatoid arthritis;signaling pathway;randomized controlled trial44|69|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06A Multicenter， Double-blind，Randomized Controlled Study of Qingfei Huatan Tongqiao Formula for Treating Adenoid Hypertrophy in Children AI Introduction
Abstract：ObjectiveTo verify the clinical efficacy of Qingfei Huatan Tongqiao Formula in treating children with adenoid hypertrophy （AH） of the lung-heat obstructing the nose syndrome， and to observe its effects on quality of life.MethodsA multicenter， double-blind， double-dummy， randomized controlled clinical trial was conducted. A total of 160 pediatric AH outpatients meeting the inclusion and exclusion criteria were enrolled between November 2022 and November 2024 from Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine， Shanghai Municipal Hospital of Traditional Chinese Medicine， Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine， and Yueyang Hospital of Integrated Traditional Chinese and Western Medicine. The children were randomly assigned to a treatment group （80 cases） or a control group 80 cases）. The treatment group received Qingfei Huatan Tongqiao Formula combined with a montelukast sodium placebo， while the control group received a Qingfei Huatan Tongqiao Formula placebo combined with montelukast sodium. The treatment course lasted 90 days. After treatment， therapeutic efficacy， sleep monitoring parameters， and Obstructive Sleep Apnea-18 （OSA-18） scores were compared between groups.ResultsCompared with pre-treatment values within each group， both groups showed significant decreases in the adenoid-to-nasopharyngeal ratio （A/N）， primary symptom scores， and TCM syndrome scores. OSA-18 scores were significantly reduced. Sleep monitoring showed decreases in the Apnea-Hypopnea Index （AHI） and Oxygen Desaturation Index （ODI）， and an increase in minimum SpO2 （all P<0.05）. After treatment， compared with the control group， the treatment group had a lower A/N ratio and higher overall effectiveness rate and TCM syndrome effectiveness rate. The treatment group also had lower total OSA-18 scores and lower subscale scores （sleep disturbance， physical symptoms， emotional distress， and caregiver impact）， with statistically significant differences （all P<0.05）. There was no significant difference in daytime symptoms （P=0.201）. Regarding sleep monitoring indices， the treatment group had lower AHI and ODI and higher minimum SpO2 （all P<0.05）， with no significant difference in average SpO2 （P=0.116）.ConclusionQingfei Huatan Tongqiao formula can significantly reduce adenoid size in children with AH， alleviate clinical symptoms， improve quality of life， reduce sleep-disordered breathing events， and ameliorate hypoxia. Its therapeutic efficacy is significantly superior to that of montelukast sodium.Keywords：Qingfei Huatan Tongqiao formula;adenoid hypertrophy;obstructive sleep apnea hypopnea syndrome;XU's pediatrics;clinical research95|67|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Clinical Efficacy of Juanbitang Hot Compress Pack Combined with Intensive Rehabilitation Training in Ameliorating Hemiplegia After Stroke AI Introduction
Abstract：ObjectiveTo explore the clinical efficacy of Juanbitang hot compress pack combined with intensive rehabilitation training in stroke patients with hemiplegia.MethodsA total of 80 stroke patients with hemiplegia were selected and assigned into a control group （40 cases） and an observation group （40 cases） according to the random number table method. The control group received conventional rehabilitation training and nursing intervention，while the observation group was additionally treated with Juanbitang hot compress pack. The two groups were compared in terms of the neurological function （national institute of health stroke scale score，NIHSS score），muscle strength，motor function （fugl-meyer assessment scale score，FMA score），daily living activity （modified barthel index，MBI），balance ability （berg balance scale score，BBS score），trunk control ability （Sheikh Trunk Control Test score，Sheikh TCT score），and homocysteine （Hcy） level before and after treatment.ResultsAfter treatment，the observation group had lower NIHSS score and Hcy level than the control group （P<0.05）. The total response rate of the observation group （97.50%） was higher than that of the control group （77.50%）. The scores of upper limb and lower limb FMA，MBI，BBS，and Sheikh TCT in the observation group were all higher than those in the control group （P<0.05）.ConclusionThe application of Juanbitang hot compress pack combined with rehabilitation training can effectively improve the neurological function，muscle strength，motor function，daily living ability，balance ability，and trunk control ability and reduce the Hcy level in stroke patients with hemiplegia，demonstrating enhanced clinical efficacy.Keywords：Juanbitang;traditional Chinese medicine hot compress pack;rehabilitation training;stroke;hemiplegia;clinical application59|54|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Effect of Huangqi Guizhi Wuwu Tang Combined with Low-molecular-weight Heparin Sodium on Preventing Deep Venous Thrombosis of Lower Extremities in Parturients Undergoing Cesarean Section Enhanced Publication AI Introduction
Abstract：ObjectiveThis paper aims to investigate the effect of Huangqi Guizhi Wuwu Tang combined with low-molecular-weight heparin sodium on preventing deep vein thrombosis of the lower extremities in parturients undergoing cesarean section.MethodsA total of 781 parturients who underwent cesarean section （from June 2022 to October 2025） were included in the study and randomly divided into a control group and an observation group using a random number table method. Two cases were lost to follow-up in this study. The parturients undergoing cesarean section in the control group （389 cases） received low-molecular-weight heparin sodium and a traditional Chinese medicine placebo （similar in color to the traditional Chinese medicine in the observation group）. The parturients in the observation group （390 cases） were treated with Huangqi Guizhi Wuwu Tang in addition to the intervention of the control group. The incidence of deep vein thrombosis of the lower extremities in parturients from both groups undergoing cesarean section， the numerical rating scale （NRS） pain scores on the first day， third day， and seventh day after cesarean section， the venous blood flow velocity in the lower extremities of parturients before and after treatment （popliteal vein， femoral vein）， the venous clinical severity score （VCSS） of parturients in the two groups after treatment， the coagulation function indicators before and after treatment ［prothrombin time（PT），activated partial thromboplastin time （APTT），fibrinogen（FIB），D-Dimer］， hemorheological indicators ［high shear viscosity（HSV），low shear viscosity（LSV），erythrocyte sedimentation rate（ESR）］， and the incidence of adverse reactions were compared.ResultsThe incidence of deep venous thrombosis in the lower extremities of parturients after cesarean section in the observation group （0.77%） was lower than that in the control group （2.83%） （χ2=4.862， P=0.031）. On the first， third， and seventh days after cesarean section， the NRS scores of the parturients in the observation group were lower than those of the control group （t=69.509， 23.266， 90.979； P<0.05 for all）. Before treatment， the venous blood flow velocities （popliteal vein， femoral vein） of the lower extremities in the parturients from the two groups were compared， and no statistical difference was found. After treatment， the venous blood flow velocities （popliteal vein， femoral vein） of the lower extremities in the parturients from these two groups increased， with higher indicator levels among the parturients in the observation group than those in the control group （t=40.492， 21.587； P<0.05 for all）. After treatment， the scores of each item in the VCSS of parturients were lower in the observation group than those in the control group （t=46.234， 37.786， 69.016， 39.464； P<0.05 for all）. Before treatment， coagulation function indicators （PT， APTT， FIB， and D-Dimer） of the parturients from the two groups were compared， and there was no statistical significance in the differences . After treatment， PT and APTT increased（P<0.05）， while FIB and D-Dimer decreased in the parturients from both groups（P<0.05）. The degrees of increase and decrease of all indicators were greater among parturients in the observation group than those in the control group （t=18.916， 12.522， 24.787， 27.635； P<0.05 for all）. Before treatment， the hemorheology indicators （HSV， LSV， ESR） in the parturients from both groups were compared， and there was no statistical significance in the differences. After treatment， these indicators in the parturients from both groups decreased， with lower indicator levels in the observation group than those in the control group （t=85.734， 26.280， 56.792； P<0.05 for all）. The incidence of adverse reactions of parturients after cesarean section in the observation group （3.85%） compared with that in the control group （3.34%）， and there was no statistically significant difference （χ²=0.143， P=0.705）.ConclusionHuangqi Guizhi Wuwu Tang combined with low-molecular-weight heparin sodium demonstrates a favorable preventive effect on deep vein thrombosis of the lower extremities in parturients undergoing cesarean section. This combined regimen improves lower extremity function， alleviates postoperative pain after cesarean section， and enhances lower-extremity blood perfusion in parturients， with safety and reliability.Keywords：caesarean section;low-molecular-weight heparin sodium;Huangqi Guizhi Wuwu Tang;deep vein thrombosis of lower extremity;coagulation function;adverse reaction78|81|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Investigation on Pharmacodynamic Material Basis of Linggui Zhugan Granules for Metabolic Associated Steatohepatitis Based on UPLC-Q-TOF-MS/MS Enhanced Publication AI Introduction
Abstract：ObjectiveTo systematically identify the main chemical components of Linggui Zhugan granules （LGZGG）， and to explore the pharmacodynamic substance basis for the treatment of metabolic dysfunction-associated steatohepatitis （MASH）.MethodsThe chemical components of LGZGG were systematically analyzed by ultra-performance liquid chromatography-quadrupole-time-of-flight tandem mass spectrometry （UPLC-Q-TOF-MS/MS）. The protein-protein interaction （PPI） network and "compound prescription-disease-component-target" network were constructed by network target analysis to predict the potential pharmacodynamic substances and core targets of LGZGG in the treatment of MASH. The potential pharmacodynamic substances were enriched by macroporous adsorption resin， and the chemical composition of the LGZGG-50% ethanol elution fraction （LGZGG-50） was analyzed by UPLC-Q-TOF-MS/MS. The mouse model of MASH was established by feeding a high-fat， high-cholesterol， and high-fructose diet for 12 weeks. Mice were randomly allocated into normal， model， positive drug （MGL-3196， 1 mg·kg-1）， LGZGG （crude drug， 34 g·kg-1·d-1）， LGZGG-50 （crude drug， 34 g·kg-1·d-1） groups. The levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） in the serum were measured， and the pathological changes in the liver tissue were observed by hematoxylin-eosin （HE） and Sirius red staining. The in vivo efficacy of LGZGG and LGZGG-50 in the treatment of MASH was evaluated on the basis of the findings. The expression levels of adenosine monophosphate-activated protein kinase （AMPK）， phosphorylated AMPK （p-AMPK）， silent information regulator 2-related enzyme 1 （SIRT1）， peroxisome proliferator-activated receptor α （PPARα）， and carnitine palmitoyltransferase 1A （CPT1A） in the liver tissue were determined by Western blot to verify the regulatory effects of core targets.ResultsA total of 83 chemical components were identified from LGZGG， including 20 flavonoids， 13 terpenoids， 17 organic acids， 7 amino acids， 11 glycosides， 3 nucleosides， 3 aromatics， 3 alkaloids， 2 phenylpropanoids， 2 sugars， 1 nucleic acid， and 1 steroid. A total of 134 common targets were obtained by network target analysis. The core targets included SIRT1， PPARα， nuclear factor-kappa B subunit 1 （NF-κB1）， and interleukin-6 （IL-6）. Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis revealed that the targets were mainly enriched in the AMPK， PPAR and other signaling pathways. The topological analysis of the "compound prescription-disease-component-target" network showed that the potential pharmacodynamic substances of LGZGG against MASH were flavonoids and terpenoids. The relative content of flavonoids and terpenes in LGZGG-50 were 74.00% and 62.41% in positive and negative ion modes， respectively， indicating that LGZGG-50 effectively enriched total flavonoids and total terpenoids. The results of in vivo efficacy showed that compared with the model group， LGZGG and LGZGG-50 reducef the body weight， liver weight， serum TG， GLU， and ALT levels of MASH mice （P<0.05，P<0.01）， and LGZGG additionally increased the HDL-C level （P<0.01）. Both groups alleviated the pathological damage in the liver tissue. The results of Western blot showed that compared with the model group， the protein levels of p-AMPK/AMPK， SIRT1， PPARα， and CPT1A were up-regulated in the LGZGG group （P<0.05，P<0.01）， and those of p-AMPK/AMPK and CPT1A were up-regulated in the LGZGG-50 group （P<0.01）.ConclusionLGZGG ameliorates MASH， with the main pharmacodynamic substances being flavonoids and terpenoids. The mechanism may be related to the regulation of AMPK/SIRT1/PPARα signaling pathway， improvement of lipid metabolism， and alleviation of pathological damage in the liver tissue.Keywords：Linggui Zhugan granules;chemical component;identification;metabolic dysfunction-associated steatohepatitis;ultra-performance liquid chromatography-quadrupole-time-of-flight tandem mass spectrometry （UPLC-Q-TOF-MS/MS）75|61|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Exploring Potential Biomarkers of Blood Stasis Syndrome in Coronary Heart Disease and Association Between Platelet Metabolic Disorder and Myocardial Injury Based on Platelet Metabolomics Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the platelet metabolomic characteristics of the rat model of coronary heart disease （CHD） with blood stasis syndrome （BSS） based on ultra-high performance liquid chromatography coupled with quadrupole-Orbitrap high-resolution mass spectrometry （UPLC-Q-Exactive Orbitrap-MS）， screen potential biomarkers and metabolic pathway information， and elucidate the association mechanism between platelet metabolic disorders and myocardial injury.MethodsA total of 12 rats were randomized into a normal group and a modle group. The rat model of CHD-BSS was established by continuous high-fat feeding， intragastric administration of vitamin D3 in divided doses combined with subcutaneous injection of isoproterenol. Additionally， changes in standard lead Ⅱ electrocardiogram （ECG） and myocardial histopathological alterations of rats in the two groups were observed to evaluate myocardial injury in the modle group. After preprocessing of the untargeted metabolomic data of platelet samples from the two groups， multivariate statistical analysis and differential screening were performed sequentially. Principal component analysis （PCA） was performed to verify the separation of metabolic profiles of samples between groups. An orthogonal partial least squares-discriminant analysis （OPLS-DA） model was then constructed to preliminarily screen potential differential metabolites based on model parameters. Secondary screening was conducted with the fold change of metabolite expression to finally identify metabolites with significant intergroup differences， and metabolic pathway enrichment analysis was carried out based on these differential metabolites. Finally， potential platelet-specific biomarkers were identified based on receiver operating characteristic（ROC） curves.ResultsCompared with the normal group， the modle group presented obvious elevation of the J point and an ST-segment elevation greater than 0.1 mV on ECG， as well as pathological injuries such as loose arrangement of fibers and cellular vacuolar degeneration in the myocardial tissue. A total of 370 differentially expressed metabolites were dysregulated in the modle group， involving 8 significantly enriched metabolic pathways，such as purine metabolism， arachidonic acid metabolism， oxidative phosphorylation and adenosine monophosphate-activated protein kinase （AMPK） signaling pathway. Nine differential metabolites enriched in these pathways showed statistically significant differences in content. ROC curve analysis revealed that the area under the curve（AUC） of all characteristic metabolites was higher than 0.8. Among them， the AUC values of four metabolites， including sphinganine 1-phosphate， sphingosine 1-phosphate， 12-ketoleukotriene B4 and 14，15-dihydroxyeicosatrienoic acid， reached 1.0， indicating their potential as biomarkers.ConclusionPlatelet metabolic characteristics are significantly altered in the rat model of CHD-BSS. The screened potential biomarkers possess favorable diagnostic performance. The pathological changes mediated by these metabolites， including inflammatory response， thrombosis， and energy metabolism disorders， serve as critical mechanisms for abnormal platelet activation and subsequent myocardial injury. Platelet metabolomics provides a new perspective for the screening of biomarkers and research on pathological mechanisms of CHD-BSS.Keywords：coronary heart disease;blood stasis syndrome;platelets;metabolomics;biomarker;myocardial injury74|51|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Hyperlipidemia Animal Models Based on Disease-syndrome Clinical Characteristics of Traditional Chinese and Western Medicine Enhanced Publication AI Introduction
Abstract：ObjectiveHyperlipidemia （HLP） is a chronic metabolic disease characterized by abnormal lipid metabolism and is one of the important risk factors for the occurrence of cardiovascular and cerebrovascular diseases. Its incidence has increased year by year， showing a trend toward younger onset. The overall prevalence of HLP among adults in China is as high as 40.40%. Although existing animal models provide important tools for research on the mechanisms of HLP， they generally show insufficient clinical concordance and lack the combined disease-syndrome characteristics of traditional Chinese medicine （TCM） and Western medicine. This article systematically reviews the research progress of HLP animal models， integrates the clinicopathological characteristics of TCM and Western medicine， and proposes new model construction strategies， aiming to provide an experimental basis for accurately analyzing the pathogenesis of HLP and developing integrated TCM-Western medicine therapies.MethodsBased on literature included in PubMed， CNKI， and Wanfang databases over the past 30 years， the construction methods and evaluation systems of HLP animal models were systematically retrieved and summarized. The concordance of existing animal models was calculated according to the new animal model evaluation method proposed by Professor MIAO Mingsan.ResultsAmong existing Western medicine modeling approaches， genetically modified models showed the highest concordance （72%）， followed by dietary induction （66%） and chemical drug induction （60%）. The dietary induction method is the most widely used in practice because of its simple operation and mature technology. Existing TCM modeling approaches are classified into three types， i.e.， spleen deficiency type， phlegm syndrome type， and liver-kidney yin deficiency type. Among them， the phlegm syndrome type shows a high degree of concordance. However， all three types have the problem of non-objective evaluation indicators and insufficient application of tongue and pulse assessment.ConclusionThe construction of existing HLP disease-syndrome combined animal models is still mainly based on Western medicine modeling methods and lacks adequate reflection of TCM syndromes. In the future， HLP animal models that conform to the clinical disease-syndrome characteristics of both TCM and Western medicine may be constructed through multifactor composite modeling strategies， intelligent tongue image analysis via robot learning， objective pulse detection， the establishment of objective evaluation systems for TCM syndromes through big data computing， and the application of cutting-edge technologies.Keywords：hyperlipidemia;animal model;integration of traditional Chinese and western medicine;combination of disease and syndrome;experimental research77|67|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Clinical Efficacy and Mechanism of Banxia Xiexin Tang-related Prescriptions in Treating Inflammation-cancer Transformation of Digestive System Based on Theory of Treating Different Diseases with Same Method： A Review Enhanced Publication AI Introduction
Abstract：Digestive system tumors are the leading cause of cancer incidence and mortality globally， and their occurrence and development generally follow the key pathological process of inflammation-cancer transformation. Therefore， intervening in the precancerous lesion stage is an important strategy to block malignant transformation of the disease and reduce the incidence rate of tumors. Banxia Xiexin Tang-related prescriptions （including Banxia Xiexin Tang， Shengjiang Xiexin Tang， and Gancao Xiexin Tang） originated from the Shanghan Zabinglun They follow the principle of pungent dispersing and bitter descending， combination of cold and warm medicinals， and tonifying deficiency and purging excess， which aligns with the core pathogenesis of digestive system precancerous lesions characterized by cold-heat intermingling and disorder of ascending and descending. These prescriptions are widely used in the clinical treatment of various digestive system inflammatory disorders such as atrophic gastritis， ulcerative colitis， and reflux esophagitis. This review systematically summarizes the theoretical basis， clinical evidence， and therapeutic mechanisms of such prescriptions in preventing and treating the inflammation-cancer transformation process in the digestive system. Clinical studies have shown that whether used alone or in combination with modern therapies， Banxia Xiexin Tang can effectively alleviate symptoms， repair histopathological changes， and improve patients' quality of life. Basic research further reveals that their efficacy stems from multi-target systemic regulatory effects： ameliorating the chronic inflammatory microenvironment， antagonizing oxidative stress， reshaping the gut microbiota， restoring the immune balance， regulating cell proliferation and apoptosis， etc. On the basis of the convergence of traditional Chinese and Western medicine understanding of inflammation-cancer transformation， this article constructs a research framework centered on regulating the inflammatory microenvironment homeostasis to systematically elucidate the mechanism of treating different diseases with the same method （Banxia Xiexin Tang）. In view of the limitations of current research in terms of evidence level， disease-syndrome combination models， and overall mechanism analysis of compound prescriptions， this article proposes future research directions of integrating high-quality clinical research， systems biology， and cutting-edge technologies， providing a new theoretical basis and translational ideas for the precise prevention and control of digestive system tumors with traditional Chinese medicine.Keywords：Banxia Xiexin Tang-related prescriptions;digestive system;inflammation-cancer transformation;mechanism study;clinical study77|62|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Molecular Mechanisms of Traditional Chinese Medicine Interventions in Cancer Based on VEGF/VEGFR Signaling Pathway： A Review Enhanced Publication AI Introduction
Abstract：Malignant tumors are major diseases with a high incidence worldwide and seriously threaten human health， and their occurrence and development are closely associated with the abnormal activation of multiple signaling pathways. Among them， the vascular endothelial growth factor （VEGF）/VEGF receptor （VEGFR） signaling pathway plays a key regulatory role in tumor angiogenesis， which can be widely implicated in tumor proliferation， invasion， and metastasis through regulating the expression of downstream signaling proteins and genes， serving as a key target for cancer targeted therapy. Traditional Chinese medicine （TCM） possesses unique advantages including multiple components， multiple targets， holistic regulation， and mild adverse reactions in cancer prevention and treatment. This paper systematically sorts out existing research findings and analyzes the anti-tumor mechanisms of TCM in modulating this signaling pathway. Furthermore， this paper summarizes that TCM active components （such as oxymatrine， quercetin， and celastrol）， extracts （such as Prunellae Spica extract and Cinnamomi Cortex extract）， and compound prescriptions （such as Yupingfeng San and modified Wenyang Sanjie Formula） can inhibit tumor angiogenesis， reverse epithelial-mesenchymal transition， improve the tumor microenvironment， promote cancer cell apoptosis， and suppress cancer cell proliferation， migration， and invasion by regulating the VEGF/VEGFR signaling pathway and its key molecules， thereby exerting anti-tumor effects. This review provides new ideas for the research and development of cancer drugs and the optimization of treatment regimens.Keywords：vascular endothelial growth factor （VEGF）/VEGF receptor （VEGFR） signaling pathway;cancer;traditional Chinese medicine （TCM） active component;TCM extract;TCM compound prescription67|46|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Traditional Chinese Medicine Regulates Immune Escape to Ameliorate Gastrointestinal Tumors： A Review Enhanced Publication AI Introduction
Abstract：Malignant gastrointestinal tumors （GT） mainly include laryngeal cancer， esophageal cancer， gastric cancer， pancreatic cancer， hepatocellular carcinoma， bile duct cancer， and colorectal cancer. At present， the morbidity and mortality of GT are high. Tumor immune escape is one of the key reasons for cancer development and treatment failure， and it is also the main direction of current tumor immunotherapy research. Traditional Chinese medicine （TCM） plays a role in treating GT and alleviating systemic symptoms， especially showing potential advantages in regulating the immune escape mechanism. This article elaborates on the immune escape mechanism of GT and systematically reviews that TCM active components or compound prescriptions act on key immune checkpoints such as programmed cell death protein-1 （PD-1） and programmed cell death ligand-1 （PD-L1） to reduce the proportion of marrow-derived suppressor cells （MDSCs）， promote the polarization of M1 macrophages， activate effector immune cells， enhance CD8+ T cell recruitment and interferon （IFN）-γ secretion， enhance the killing activity of natural killers （NKs）， and reduce foxhead box protein P3（FoxP3+）-positive regulatory T （Treg） cell infiltration. TCM active components or compound prescriptions can remodel the tumor microenvironment （TME）， such as improving immunosuppressive factors， promoting vascular normalization， and regulating intestinal microbiota. Through the regulation of TME， enhancement of antigen presentation， inhibition of immune checkpoint molecules， regulation of cellular network factors and metabolites， etc.， TCM active components or compound prescriptions enhance the immune function， thereby inhibiting the immune escape of GT. This paper summarizes and reflects on the research results of TCM in regulating immune escape to treat GT in recent years， aiming to help transform TCM from empirical medication to precision treatment based on immune regulation， reduce drug resistance and enhance treatment effect.Keywords：gastrointestinal tumor;immune escape;traditional Chinese medicine （TCM） active component;TCM compound prescription;mechanism of action70|78|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Traditional Chinese Medicine Modulates Endoplasmic Reticulum Stress for Prevention and Treatment of Neuropathic Pain： A Review Enhanced Publication AI Introduction
Abstract：Neuropathic pain （NP） is a chronic pain syndrome resulting from injury， inflammation， or dysfunction of the somatosensory nervous system. Its pathogenesis is complex and intimately associated with peripheral sensitization and maladaptive neuroplasticity within the central nervous system. The core clinical manifestations， including spontaneous pain， allodynia， and paresthesia， severely compromise patients’ quality of life and pose substantial challenges to clinical management. Endoplasmic reticulum stress （ERS）， a critical cellular defense mechanism against disrupted intracellular homeostasis， is primarily initiated and modulated through three canonical branches of the unfolded protein response （UPR）： the protein kinase RNA-like endoplasmic reticulum kinase （PERK） pathway， the inositol-requiring transmembrane kinase/endonuclease 1α （IRE1α） pathway， and the activating transcription factor 6 （ATF6） pathway. These signaling cascades play a pivotal role in the pathological progression of NP. Traditional Chinese medicine （TCM） exhibits unique advantages in the treatment of NP. Leveraging its hallmark characteristics of multi-target， multi-pathway， and holistic regulation， TCM can systematically modulate the ERS signaling network to inhibit neuronal apoptosis， attenuate neuroinflammatory infiltration， and rectify autophagic dysfunction， ultimately promoting the repair and regeneration of damaged neural tissue. This review systematically summarizes the core role of ERS in the occurrence and development of NP. It focuses on the latest research progress regarding ERS pathway modulation in NP amelioration by representative TCM interventions， including potential core bioactive components （e.g.， tanshinoneⅡA， catalpol， and formononetin）， classic and empirical compound formulas （e.g.， Huangqi Guizhi Wuwu decoction， Compound Qiying granules， and Tangluoning）， and TCM external therapies （e.g.， electroacupuncture， moxibustion with seed-sized moxa cone， and acupotomy）. Through an in-depth analysis of the functional characteristics and mechanisms of these TCM interventions， particularly their bidirectional regulation and multi-target synergy， this review aims to provide a solid theoretical foundation for further optimizing TCM-based strategies for NP prevention and treatment and to delineate future directions for clinical translation of related research achievements and targeted drug development.Keywords：endoplasmic reticulum stress;neuropathic pain;research progress;traditional Chinese medicine;mechanism74|54|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Traditional Chinese Medicine Regulates NF-κB Signaling Pathway for Treating CP/CPPS： A Review Enhanced Publication AI Introduction
Abstract：Chronic prostatitis/chronic pelvic pain syndrome （CP/CPPS） is a prevalent and complex condition in urology and one of the leading causes of chronic pelvic pain. Due to its prolonged duration and recurrent episodes，CP/CPPS significantly impacts patients' quality of life. Abnormal activation of the nuclear transcription factor-κB （NF-κB） pathway influences pathological processes such as the inflammatory response，oxidative stress，apoptosis，and tissue fibrosis in the body，thereby promoting the progression of CP/CPPS. Currently，Western medical therapies include antibiotics，pain relievers，α-blockers，and physiotherapy，yet they still fail to halt the pathological process of CP/CPPS. Research indicates that traditional Chinese medicine （TCM） can modulate the NF-κB pathway through a multi-target and multi-pathway approach，effectively reducing prostate tissue damage and prostate index and alleviating pain and lower urinary tract symptoms. On the basis of existing studies，this paper systematically examines the intrinsic connection between CP/CPPS and the NF-κB pathway and summarizes the effects of TCM active ingredients （e.g.，emodin，quercetin，and gentiopicroside），extracts （e.g.，Oldenlandia diffusa extract），classical medidcinal pairs （e.g.，Phellodendri Chinensis Cortex-Smilacis Glabrae Rhizoma），and compound prescriptions and Chinese patent medicines （e.g.，Qianliexiao decoction，Jiedu Huoxue decoction，Qianlie Shutong capsules） in treating CP/CPPS by regulating the NF-κB signaling pathway. The review of the research findings on treating CP/CPPS through this pathway aims to offer insights for clinical practice of TCM in the prevention and treatment of CP/CPPS，as well as to provide references for basic research and new drug development in this domain.Keywords：chronic prostatitis;chronic pelvic pain syndrome;nuclear factor （NF）-κB signaling pathway;traditional Chinese medicine;research progress70|30|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Traditional Chinese Medicine Interventions in Oligoasthenospermia-related Signaling Pathways： A Review Enhanced Publication AI Introduction
Abstract：Oligoasthenospermia （OAS） is the common cause of male infertility，bringing fertility problems to many families. Its pathogenesis is complex，involving endocrine disorders，reproductive system infection，oxidative stress injury，immune dysfunction and other aspects. At present，the Western medicine treatment of OAS is mainly based on drugs，surgery，and assisted reproductive technology. However，drug therapy has certain side effects，and long-term use is easy to produce drug resistance. Surgical treatment has certain trauma and risk. Assisted reproductive technology is not widely available because of its high cost. Therefore，there is an urgent need to develop safer，economical，and effective treatment options. Traditional Chinese medicine （TCM） has obvious advantages in the treatment of OAS. It can play a role in the treatment of OAS by reducing oxidative stress，inhibiting inflammatory response，reducing apoptosis，and regulating cell autophagy through multiple pathways and targets. Recent studies have shown that TCM compound prescriptions，single medicinal materials，medicinal pairs，and their active components can ameliorate OAS by regulating several key signaling pathways such as the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） pathway，Janus kinase 2/signal transducer and activator of transcription 3（JAK2/STAT3） pathway，nuclear factor E2-related factor 2/heme oxygenase-1 （Nrf2/HO-1） pathway，stem cell factor/tyrosine kinase receptor （SCF/c-kit） pathway，nuclear factor-κB （NF-κB） pathway，transforming growth factor-β （TGF-β）/Smads pathway，and extracellular regulated protein kinase （ERK） pathway. This article summarizes the role of the above signaling pathways in the occurrence and development of OAS and the therapeutic mechanism of TCM，aiming to provide a scientific basis for the clinical treatment of OAS and the research and development of drugs.Keywords：oligoasthenospermia;male infertility;traditional Chinese medicine;signaling pathway;research progress86|43|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Mechanisms of Action of Angelica sinensis in Prevention and Treatment of Alzheimer's Disease： A Review Enhanced Publication AI Introduction
Abstract：Alzheimer's disease （AD） is a chronic neurodegenerative disorder with an unclear pathogenesis and currently no cure. It is characterized by a long disease course， diverse symptoms， and a persistent， difficult-to-treat nature， which greatly affects the quality of life of elderly patients. Traditional Chinese medicine （TCM） offers significant advantages in the treatment of AD， featuring multi-component， multi-target， and multi-pathway characteristics， with few adverse reactions and good safety. Angelica sinensis is a commonly used medicinal herb. As a frequently used clinical medicine for nourishing and activating blood， it shows significant efficacy in treating blood deficiency syndrome. In recent years， studies have revealed that A. sinensis exhibits significant activity in the prevention and treatment of AD. It contains various active components such as organic acids， volatile oils， and polysaccharides， and possesses pharmacological effects including anti-inflammatory， antioxidant， hepatoprotective， and neuroprotective properties. This article summarizes and outlines the mechanisms of A. sinensis and its compound formulas in the prevention and treatment of AD， providing a reference for its clinical application and the treatment of AD.Keywords：Angelica sinensis;Alzheimer's disease;compound formulas;active ingredient;molecular mechanisms92|66|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06Chemical Constituents and Pharmacological Effect of Euodiae Fructus： A Review Enhanced Publication AI Introduction
Abstract：Euodiae Fructus， a commonly used Chinese medicinal herb， has been widely used to treat gastrointestinal disorders， headaches， and vomiting， possessing significant medicinal value. According to traditional Chinese medical theory， Euodiae Fructus has the following effects： warming the middle to disperse cold， suppressing adverse Qi to relieve vomiting， and soothing the liver to alleviate pain. It is commonly used to treat diseases associated with cold stagnation in the liver and stomach， as well as gastrointestinal dysfunction. In recent years， as modern research on traditional Chinese medicine has advanced， increasing attention has been paid to the chemical constituents and pharmacological effects of Euodiae Fructus. Studies have isolated and identified various chemical constituents in this herb， including alkaloids， terpenoids， phenols， steroids， and volatile oils. Among them， alkaloids and terpenoids have been most extensively investigated. Studies suggest that Euodiae Fructus and some of its active constituents exhibit anti-inflammatory， anti-tumor， cardiovascular and cerebrovascular protective， and metabolic syndrome-regulating effects. However， current studies mainly focus on a few representative constituents. A systematic understanding of the overall bioactive material basis and mechanisms of action of this herb still requires further investigation. Additionally， more in vivo pharmacodynamic studies， clinical evaluations， and toxicological assessments are needed. This article summarizes recent advances in the pharmacological effects of Euodiae Fructus based on a systematic review of its major chemical constituents， aiming to provide a reference for further research and the rational development and utilization of this medicinal herb.Keywords：Euodiae Fructus;chemical constituent;pharmacological effect;mechanism of action;toxicity and safety170|82|0<HTML><H-PDF> <L-PDF>Updated：2026-08-06
