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Online FirstList of IssuesDocument Types
- Abstract：ObjectiveTo observe the effects of modified Longdan Xiegan Tang on wound healing and inflammatory factors after surgery for perianal abscess of heat-toxin accumulation syndrome.MethodsA prospective randomized controlled design was adopted. A total of 110 patients with perianal abscess of heat-toxin accumulation syndrome admitted to Hebei Provincial Hospital of Traditional Chinese Medicine from January 2024 to January 2025 were included and randomly assigned into two groups， each with 55 patients according to the random number table method. The control group received conventional Western medicine treatment + placebo oral administration after surgery， and the observation group received modified Longdan Xiegan Tang oral administration on the basis of conventional Western medicine treatment， with a course of 14 days. Clinical efficacy， Visual Analogue Scale （VAS） score， wound secretion score， TCM symptom score， wound healing rate， wound healing time， wound infection rate， inflammatory factors ［interleukin-6 （IL-6）， interleukin-8 （IL-8）， and tumor necrosis factor-α （TNF-α）］， wound healing-related indicators ［fibronectin （FN）， matrix metalloproteinase-9 （MMP-9）， and prealbumin （PA）］ and adverse reactions were determined in both groups.ResultsThree cases in the observation group and three cases in the control group dropped out， with 104 cases actually completing the study. The repeated measures analysis of variance showed that both groups showed decreased VAS scores， wound secretion scores， TCM syndrome scores， and levels of IL-6， IL-8， TNF-α， and MMP-9 and increased levels of PA and FN after treatment （P<0.05）. During treatment and on day 14 after surgery， the observation group had lower VAS score， wound secretion score， TCM syndrome score， and levels of IL-6， IL-8， TNF-α， and MMP-9 and higher levels of PA and FN than the control group （P<0.01）. The observation group showed higher wound healing rate， shorter wound healing time， and lower wound infection than the control group （P<0.01）. The comprehensive efficacy of the observation group was better than that of the control group （χ2=5.216， P<0.05）. No serious adverse events occurred in patients during the study， and there was no significant difference in the incidence of adverse reactions between the two groups.ConclusionModified Longdan Xiegan Tang can ameliorate wound condition， reduce inflammatory response， and promote wound healing in patients with perianal abscess of heat-toxin accumulation syndrome after surgery， with good safety.Keywords：modified Longdan Xiegan Tang;heat-toxin accumulation syndrome;perianal abscess;wound healing;inflammatory factors;Fibronectin34|7|0
<HTML><H-PDF><L-PDF>Updated：2026-08-31 - Abstract：ObjectiveTo investigate the synergistic promotion of malignant phenotypes in gastric cancer cells by tumor-associated bone marrow mesenchymal stem cells （TA-BMSCs） and polymorphonuclear myeloid-derived suppressor cells （PMN-MDSCs） through crosstalk， and the intervention mechanism of the intestinal absorption solution containing Banxia Xiexin Tang （BXT）.MethodsGastric cancer MFC cells were treated with conditioned medium （co-culture-CM） prepared from a co-culture system of TA-BMSCs and PMN-MDSCs. Groups included control， co-culture-CM model， stromal cell-derived factor 1 （SDF1） inhibitor （LY2510924）， α4β1 inhibitor （BIO5192）， dual inhibitor combination， and different concentrations （55%， 70%， and 85%） of BXT-containing intestinal absorption solutions. MFC cell proliferation， migration， invasion， and apoptosis were assessed via cell counting kit-8 （CCK-8） assay， wound-healing assay， Transwell assay， and flow cytometry. The SDF-1， α4β1， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA） levels in culture supernatants， along with the protein levels of intracellular macrophage migration inhibitory factor （MIF）， chemokine （C-X-C motif） receptor 4 （CXCR4）， CD106， MMP-9， and VEGFA in MFC cells， were measured by enzyme-linked immunosorbent assay （ELISA） and Western blot， respectively.ResultsCompared with the control group， co-culture-CM promoted the proliferation， migration， and invasion of MFC cells （P<0.01）， elevated the levels of SDF-1， α4β1， MMP-9， and VEGFA （P<0.01）， and upregulated the protein levels of MIF （P<0.05）， MMP-9 （P<0.01）， and VEGFA （P<0.01）. Compared with co-culture-CM， BXT-containing intestinal absorption solutions at various concentrations significantly reversed the phenotypic effects on cells， inhibited malignant phenotypes， lowered the levels of MMP and SDF1， and reduced the expression of proteins in the crosstalk axis. Compared with the SDF1+α4β1 inhibitor group， the SDF1 inhibitor group and the α4β1 inhibitor group showed no differences in the inhibition of proliferation， scratch healing， and cytokine levels. The SDF1 inhibitor increased the apoptosis rate and downregulated the protein levels of MIF and CD106， while the α4β1 inhibitor increased the number of migrated cells and the expression of various proteins. Compared with the SDF1 inhibitor group， the α4β1 inhibitor group showed reduced inhibitory effect on proliferation， decreased apoptosis rate， increased number of invasive cells， decreased α4β1 content， and increased expression of various proteins （P<0.01）. The 55%， 70%， and 85% intestinal absorption solutions increased the inhibitory effect on proliferation， decreased the number of invasive cells， and increased the apoptosis rate （P<0.01）. The 55% BXT-containing intestinal absorption solution group showed increased wound healing rate and upregulated protein levels of VEGFA， CD106， and MMP-9 （P<0.05）. The 70% intestinal absorption solution group showed upregulated protein level of MIF （P<0.05）， and the 85% intestinal absorption solution group showed upregulated protein level of VEGFA （P<0.01） and downregulated the protein level of CXCR4 （P<0.01）.ConclusionTA-BMSCs and PMN-MDSCs synergistically activate the MIF/SDF-1/CXCR4 and MMP-9/α4β1/CD106 axes through crosstalk， significantly enhancing gastric cancer cell invasion and migration. BXT-containing intestinal absorption fluid effectively inhibits the malignant progression of gastric cancer cells by multi-targeted intervention in this crosstalk process.Keywords：Banxia Xiexin Tang;drug-containing intestinal absorption solution;tumor-associated bone marrow mesenchymal stem cells;polymorphonuclear myeloid-derived suppressor cells;cell crosstalk30|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
- Abstract：ObjectiveTo explore whether the intestinal absorption solution containing Banxia Xiexintang （BXT） can inhibit the invasion and migration of gastric cancer cells by interfering with the stromal cell-derived factor 1 （SDF1）-CXC chemokine receptor 4 （CXCR4） axis in tumor-associated bone marrow mesenchymal stem cells （TA-BMSCs）.MethodsThe intestinal absorption solution containing BXT was prepared， and the optimal intervention concentration and duration for MFC cells were determined through the cell counting kit-8 （CCK-8） assay. A co-culture system was established comprising TA-BMSCs conditioned medium （TA-BMSCs-CM） and gastric cancer MFC cells. The experiment was conducted with a blank control group， a TA-BMSCs-CM group， an SDF1 inhibitor （LY2510924） group， and intervention groups with varying concentrations （55%， 70%， and 85%） of the intestinal absorption solution containing BXT. Cell proliferation was assessed by the CCK-8 assay. Horizontal and vertical cell migration were evaluated via scratch and Transwell assays， respectively. Cell invasion was examined by a Transwell assay with Matrigel. Cell apoptosis was detected by flow cytometry. The levels of factors such as SDF1， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA）， as well as the protein levels of macrophage migration inhibitory factor （MIF）， CXCR4， VEGFA， and MMP-9， were quantified by ELISA and Western blot， respectively.ResultsThe CCK-8 assay results indicated that compared with the 24 h intervention， the 48-h interventions with all concentrations of the intestinal absorption solution containing BXT increased the inhibition rate on MFC cells （P<0.01）. The half-maximal inhibitory concentration （IC50） of the intestinal absorption solution containing BXT at the time point of 48 h was 68.51%， and subsequent intervention concentrations were selected as 55%， 70%， and 85%. Compared with the TA-BMSCs-CM group， the intestinal absorption solution containing BXT （particularly at concentrations of 70% and 85%） suppressed the proliferation， migration， and invasion of MFC cells， promoted the cell apoptosis （P<0.05， P<0.01）， decreased the levels of SDF1， MMP-9， and VEGFA， and downregulated the protein levels of MIF， CXCR4， VEGFA， and MMP-9 （P<0.05， P<0.01）. The inhibitory effects of the intestinal absorption solution containing BXT were comparable to or superior to those of the SDF1 inhibitor （P<0.01）.ConclusionThe intestinal absorption solution containing BXT can inhibit the invasion and migration of gastric cancer cells by interfering with the SDF1-CXCR4 axis in TA-BMSCs. The underlying mechanism may involve the regulation of the MIF/SDF-1/CXCR4 signaling pathway and its downstream effector molecules.Keywords：Banxia Xiexintang;drug-containing intestinal absorption solution;tumor-associated bone marrow mesenchymal stem cells;cell crosstalk25|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
Exploring Pathogenesis and Treatment of Gastric Cancer Metastasis Based on Blood Harmonizing Method AI Introduction
Abstract：Metastasis in gastric cancer is a key factor contributing to poor prognosis. Its pathogenesis is complex， characterized by a combination of underlying deficiency and superficial excess， cold and heat in complexity， and stagnation in collateral Conventional aggressive treatment methods tend to exacerbate the depletion of healthy Qi and Zang-Fu organ dysfunctions. The harmonizing method in traditional Chinese medicine （TCM） emphasizes holistic regulation and reinforcing healthy Qi while expelling pathogenic factors. The blood harmonizing method is grounded in the core TCM theory of blood vessel transmission and Zang-Fu organ accumulation of cancerous toxins. It closely addresses the essence of metastasis—where cancerous toxins spread through the bloodstream and accumulate in the collaterals-thereby providing a unique and feasible diagnostic and therapeutic approach for clinical intervention in gastric cancer metastasis. This paper systematically reviews relevant TCM theories such as transmission and Zang-Fu organ accumulation of cancerous toxins and accumulation-gathering and provides an in-depth explanation of the core pathogenesis of gastric cancer metastasis. Specifically， cancerous toxins circulate throughout the body via the blood vessels and accumulate in the collaterals of target organs such as the liver， peritoneum， lymph nodes， and lungs. The occurrence and development of this process are consistently centered on the key mechanism of disharmony in blood-related syndromes. On this basis， the paper explicitly proposes three major therapeutic approaches centered on harmonizing the blood. The first is harmonizing the blood to restore ascending and descending functions， thereby invigorating the spleen and regulating the middle energizer to restore the mediating function of the middle energizer and block the generation of phlegm and blood stasis at the root. The second is harmonizing the blood to balance cold and heat， using pungent herbs to open and bitter herbs to descend to harmonize the Yin-Yang balance and improve the homeostasis of the tumor microenvironment. The third is harmonizing the blood to unblock collaterals and resolve stasis， thereby gradually dissipating stasis and nodules， gently clearing obstructions in the collaterals， and breaking the critical link of collateral stagnation forming masses caused by metastasis. The article further summarizes modern pharmacological research findings on representative formulas such as Banxia Xiexintang， Weichang An， Yangzheng Sanjie decoction， and Sijunzitang， confirming that they can inhibit the proliferation， invasion， and metastasis of gastric cancer cells， as well as epithelial-mesenchymal transition， through multiple targets and pathways， to regulate angiogenesis and lymphangiogenesis， modulate the immune microenvironment， and induce tumor cell apoptosis and ferroptosis， thereby blocking the metastasis process at multiple levels. This paper discusses the theoretical basis， pathogenetic mechanisms， therapeutic systems， and modern mechanisms of the blood harmonizing method for the diagnosis and treatment of gastric cancer metastasis. It fully embodies the TCM principles of targeting balance， reinforcing healthy Qi without aiding the pathogen， and eliminating the pathogen without harming the healthy Qi， providing a solid theoretical foundation and practical pharmacological references for the prevention and treatment of gastric cancer metastasis with integrated traditional Chinese and Western medicine in clinical practice.Keywords：harmonizing blood;gastric cancer metastasis;peritoneal metastasis;blood vessels;therapeutic method15|5|0<HTML><H-PDF><L-PDF>Updated：2026-08-31- Abstract：Diabetic kidney disease （DKD）， a prevalent microvascular complication of diabetes mellitus， is characterized by intricate pathophysiological mechanisms and persistent clinical management challenges. Historically， glomerular injury has been regarded as the central pathological hallmark of DKD， with research predominantly focusing on hyperfiltration， glomerular basement membrane thickening， and podocyte dysfunction. Emerging evidence， however， underscores the renal tubule—not merely as a passive bystander but as an early initiator and pivotal driver—in DKD pathogenesis. Hyperglycemia， metabolic dysregulation， and chronic low-grade inflammation induce tubular epithelial cell injury at early disease stages. Such injury disrupts tubuloglomerular feedback， thereby elevating intraglomerular pressure and sustaining hyperfiltration. Concurrently， injured tubular cells secrete pro-inflammatory cytokines and profibrotic factors， promoting epithelia-mesenchymal transition， interstitial hypoxia， and progressive tubulointerstitial fibrosis that ultimately culminate in irreversible decline of renal function. This “tubule-first” paradigm represents a fundamental shift from the classical glomerulocentric model and redefines the conceptual framework of DKD progression. Traditional Chinese medicine， with its inherent advantages of multi-component synergy， multi-target engagement， and systemic homeostatic regulation， has demonstrated compelling renoprotective effect， particularly in preserving tubular integrity and function， mitigating tubular cellular stress， and indirectly alleviating glomerular hemodynamic burden. Accumulating preclinical and clinical evidence supports the efficacy of numerous single herbs and standardized formulae of TCM in attenuating tubulointerstitial injury and slowing down DKD progression. This review systematically delineates the sequential pathogenic cascade—from initial tubular insult to secondary glomerular deterioration—and critically evaluates the mechanism basis and translational potential of TCM-based interventions targeting tubular resilience. We aim to provide a refined pathophysiological rationale and actionable insights for optimizing clinical strategies and accelerating the development of novel therapeutics for DKD.Keywords：diabetic kidney disease;renal tubule;glomerulus;tubuloglomerular feedback;traditional Chinese medicine20|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
Nose-to-brain Delivery of Traditional Chinese Medicine Essential Oils for Neurological Disorders： Applications and Molecular Mechanisms AI Introduction
Abstract：The nose-to-brain pathway refers to a significant drug delivery route through which substances traverse the unique anatomical structures of the nasal cavity to directly access the central nervous system， bypassing the blood-brain barrier. Its core advantage lies in utilizing the olfactory and trigeminal nerves， enabling peripheral drug administration to rapidly and efficiently reach the brain， thereby avoiding the drug loss and bioavailability reduction associated with oral or intravenous routes due to the circulatory system and blood-brain barrier limitations. In recent years， with in-depth research into the neuroanatomy of the olfactory system， nasal mucosal barrier properties， and neural regulatory mechanisms， the potential application of the nose-to-brain pathway in neurological diseases has attracted increasing attention. Traditional Chinese medicine （TCM） essential oils， characterized by strong lipophilicity， small molecular weights， volatility， and diverse chemical components， are highly compatible with the physiological characteristics of the nose-to-brain pathway， thus serving as promising carriers for brain-targeted drug delivery， enhancing drug bioavailability， and exerting neuroprotective effects. On this basis， this review systematically summarizes the anatomical and physiological bases for the delivery of TCM essential oils via the nose-to-brain pathway， the patterns of drug transport and brain distribution， clinical and animal study examples in neurological diseases， the associated molecular mechanisms and signaling pathways， and the progress in the development of novel nasal essential oil formulations. Additionally， the review analyzes the current challenges in this field and proposes strategies for future research and application. By systematically discussing the nose-to-brain pathway and the delivery mechanisms of TCM essential oils， this study aims to provide theoretical support for drug development， mechanism exploration， and formulation innovation in the treatment of neurological diseases， while also offering scientific guidance for further research and clinical applications of the nose-to-brain delivery system.Keywords：essential oils;nose-to-brain pathway;drug delivery;neurological disease;signaling pathway25|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31Efficacy of Tanreqing Gel in Treating Acne and Its Effect on TLR2/MyD88/NF-κB Signaling Pathway AI Introduction
Abstract：ObjectiveTo explore the pharmacological mechanism of Tanreqing Gel （TRQG） in the treatment of acne by regulating the Toll-like receptor 2 （TLR2）/myeloid differentiation 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway.MethodsThe minimum inhibitory concentration （MIC） of Tanreqing injection （TRQ） against Cutibacterium acnes was determined through the microdilution broth method， and drug resistance induction experiments were conducted. A mouse model of acne was established through inoculation of C. acnes on the back. The effects of TRQG on skin structure， pustule formation， collagen repair， and inflammatory response were evaluated by dermoscopy， histopathology， two-photon excitation fluorescence microscopy （TPEF）， and optical coherence tomography （OCT）. Differentially expressed genes （DEGs） were identified through transcriptome sequencing and then subjected to KEGG pathway enrichment analysis. In the RAW264.7 cell model， the optimal dosage of TRQG was determined through cell viability assays. Subsequently， the expression of key proteins in the TLR2/MyD88/NF-κB pathway and downstream inflammatory factors ［tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， and IL-6］ was determined by Western blot and real-time PCR.ResultsThe MIC of TRQ against C. acnes was 4 125 mg·L-1. Although TRQ had weaker antibacterial activity than erythromycin （ERY） and fusidic acid （FA）， it was less likely to induce bacterial resistance. In vivo experiments showed that TRQG improved the skin structure， promoted collagen repair （P<0.01）， inhibited pustule formation （P<0.01）， alleviated follicular keratinization and sebaceous gland hyperplasia， and reduced inflammatory responses in the mouse model of acne compared with erythromycin gel （ERYG）. Transcriptome analysis suggested that the TLR/MyD88/NF-κB signaling pathway was a key enriched pathway. Further experimental validation indicated that TRQG inhibited the expression of TLR2， MyD88， TNF receptor-associated factor 6 （TRAF6）， phosphorylated （p）-transforming growth factor-β-activated kinase 1 （TAK1）， p-inhibitor of NF-κB subunit α （IκBα）， and p-NF-κB in this pathway （P<0.01）. Meanwhile， real-time PCR results confirmed that TRQG reduced the mRNA levels of TNF-α， IL-1β， and IL-6 （P<0.01）.ConclusionTRQG exerts its therapeutic effect on acne by inhibiting the activation of the TLR2/MyD88/NF-κB signaling pathway and reducing the release of downstream inflammatory factors. Furthermore， it is less likely to induce bacterial resistance， indicating a promising application prospect.Keywords：Tanreqing Gel;acne;Cutibacterium acnes;Toll-like receptor 2 （TLR2）/myeloid differentiation 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway;anti-inflammatory mechanism18|9|0<HTML><H-PDF><L-PDF>Updated：2026-08-31- Abstract：ObjectiveThis study aimed to evaluate the effects of cycloastragenol （CAG） on mitochondrial dysfunction during cardiac remodeling and to elucidate its regulatory role in myocardial energy metabolic homeostasis and the associated transcriptional regulatory axis.MethodsA rat model of heart failure （HF） was established by ligation of the left anterior descending coronary artery. Rats were randomly divided into a control group， a model group， a captopril group （3.25 mg·kg-1）， a low-dose CAG group （10 mg·kg-1， CAG-L）， and a high-dose CAG group （20 mg·kg-1， CAG-H）. After 28 days of treatment， left ventricular ejection fraction （LVEF）， left ventricular fractional shortening （LVFS）， left ventricular end-diastolic diameter （LVIDd）， and left ventricular end-systolic diameter （LVIDs） were assessed by echocardiography. Serum levels of N-terminal pro-brain natriuretic peptide （NT-proBNP）， creatine kinase-MB （CK-MB）， cardiac troponin I （cTnI）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and cyclic adenosine monophosphate （cAMP） were measured by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） and Masson's trichrome staining were used to evaluate myocardial histopathology and fibrosis. Wheat germ agglutinin （WGA）， reactive oxygen species （ROS）， and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining were performed to assess cardiomyocyte hypertrophy， oxidative stress， and apoptosis. Adenosine triphosphate （ATP） content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ were determined by colorimetric assays. The mRNA expression of α-smooth muscle actin （α-SMA）， Col Ⅰ， and Col Ⅲ was detected by real-time quantitative polymerase chain reaction （RT-qPCR）， while the protein levels of β₂-adrenergic receptor （ADRB2）， protein kinase A （PKA）， phosphorylated cAMP response element-binding protein/total cAMP response element-binding protein （p-CREB/CREB）， peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）， nuclear respiratory factor 1 （NRF1）， and mitochondrial transcription factor A （TFAM） were analyzed by Western blot.ResultsCompared with the control group， the model group exhibited significantly decreased LVEF， LVFS， and ATP levels （P<0.05）， and markedly increased LVIDd， LVIDs， NT-proBNP， CK-MB， cTnI， IL-1β， IL-6， TNF-α， ROS levels， TUNEL-positive rate， Col deposition area， and the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ （P<0.05）. In addition， the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， the protein expression of ADRB2， PKA， p-CREB， PGC-1α， NRF1， and TFAM， as well as the cAMP content， were significantly reduced （P<0.05）. Compared with the model group， both low- and high-dose CAG significantly increased LVEF and LVFS， and decreased LVIDd， LVIDs， and the levels of NT-proBNP， CK-MB， and cTnI （P<0.05）. CAG treatment alleviated myocardial disarray and Collagen deposition， and downregulated the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ. The treatment markedly reduced ROS generation and the TUNEL-positive rate （P<0.05）， thereby attenuating cardiomyocyte hypertrophy and inflammatory responses. Furthermore， CAG treatment increased ATP content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， accompanied by upregulation of PGC-1α， NRF1， TFAM， ADRB2， PKA， and p-CREB protein expression as well as cAMP levels （P<0.05）. The CAG-H group showed the most pronounced improvements， which were superior to those of the captopril group and the CAG-L group.ConclusionCycloastragenol delays adverse cardiac remodeling and improves cardiac function by activating the ADRB2-mediated GPCR/cAMP/PKA/CREB signaling pathway， enhancing the PGC-1α/NRF1/TFAM activity， promoting mitochondrial energy metabolism remodeling， and suppressing oxidative stress， inflammation， and myocardial fibrosis.Keywords：cycloastragenol;heart failure;G protein-coupled receptor/cyclic adenosine monophosphate/protein kinase A/cAMP response element-binding protein （GPCR/cAMP/PKA/CREB）;peroxisome proliferator-activated receptor γ coactivator-1α/nuclear respiratory factor 1/mitochondrial transcription factor A （PGC-1α/NRF1/TFAM）;mitochondrial function;cardiac remodeling21|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
Effect of Yinqi Sanhuang Jiedu Decoction on Piezo1-YAP Signaling Axis and Macrophage Polarization in Mouse Model of Liver Fibrosis AI Introduction
Abstract：ObjectiveTo validate the therapeutic effect of Yinqi Sanhuang Jiedu decoction （YQSH） on a mouse model of carbon tetrachloride （CCl4）-induced liver fibrosis and to investigate its correlations with the Piezo-type mechanosensitive ion channel component 1 （Piezo1）-Yes-associated protein （YAP） mechanical signaling axis and macrophage polarization.MethodsFifty-four C57BL/6J mice were randomized into a blank control group， a 4-week model group， a 6-week model group， a 8-week model group， a positive drug （silymarin， 55 mg·kg-1·d-1） group， and low-， medium-， and high-dose （8.325， 16.65， and 33.3 g·kg-1·d-1， respectively） YQSH groups. Except the 6-week model group （n=12）， each of the other groups had 6 mice. Mice in other groups except the blank control group received intraperitoneal injections of 10% CCl4 twice weekly for the modeling of liver fibrosis. Drug interventions began one week after the initial modeling through gavage， and the blank control and model groups received 0.2 mL of normal saline via gavage. The histopathological changes and collagen deposition in the liver were observed via hematoxylin-eosin （HE）， Masson's trichrome， and Sirius red staining. Serum activities of alanine aminotransferase （ALT） and aspartate aminotransferase （AST）， as well as serum levels of total protein （TP）， albumin （ALB）， total bilirubin （TBIL）， hyaluronic acid （HA）， laminin （LN）， procollagen type Ⅲ （PCⅢ）， and collagen type Ⅳ （Ⅳ-C）， were measured. The levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in the liver tissue were determined by enzyme-linked immunosorbent assay （ELISA）. The protein and mRNA levels of Piezo1 and YAP1 in the liver tissue were determined by immunohistochemistry （IHC） and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. Co-localization of Piezo1 with YAP1， and YAP1 with inducible nitric oxide synthase （iNOS） was observed by the immunofluorescence （IF） assay. The proportions of M1-type （F4/80+CD80+） and M2-type （F4/80+CD206+） macrophages in the liver tissue were examined by flow cytometry. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analyses and gene set enrichment analysis （GSEA） were performed through transcriptomic sequencing.ResultsCompared with the blank control group， the model group exhibited gradually worsened liver fibrosis at the 4th， 6th， and 8th weeks. The 6- and 8-week model groups showcased inflammatory cell infiltration and collagen deposition in the liver （P<0.01） and upregulated protein levels of both Piezo1 and YAP1 （P<0.01）. Compared with the model groups， treatment with YQSH improved the liver function （P<0.05， P<0.01）， alleviated liver fibrosis （P<0.05， P<0.01）， and reduced intrahepatic inflammatory cell infiltration and collagen deposition （P<0.01）. Furthermore， the treatment downregulated the protein and mRNA levels of Piezo1 and YAP1 （P<0.05， P<0.01）， lowered the levels of inflammatory factors TNF-α and IL-1β （P<0.05， P<0.01）， and decreased the ratio of CD80 （M1-type）/CD206 （M2-type） macrophage proteins （P<0.01）. The IF assay showed co-localization of YAP1 with Piezo1 and iNOS. Compared with the model groups， YQSH treatment downregulated the expression of Piezo1， YAP1， and iNOS （P<0.05， P<0.01）. Transcriptomic analysis suggested that the anti-liver fibrosis effect of YQSH may be related to the Hippo signaling pathway （P<0.05）.ConclusionThe anti-liver fibrosis effect of YQSH may be related to its inhibition of the Piezo1-YAP signaling axis and regulation of macrophage polarization.Keywords：liver fibrosis;Yinqi Sanhuang Jiedu decoction;Piezo-type mechanosensitive ion channel component 1 （Piezo1）;Yes-associated protein 1 （YAP1）;macrophage polarization25|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31- Abstract：ObjectiveTo investigate the effect and mechanism of Banxia Shumitang plus Zhizichi Tang （BZ） on PTEN-induced kinase 1 （PINK1）/Parkin signaling pathway in regulating mitochondrial autophagy in preventing insomnia with depression.MethodsSeventy-two 6-week-old male Kunming mice were randomized into a normal group， a model group， low-dose， medium-dose， and high-dose BZ groups （BZ-L， BZ-M， BZ-H， 2.92， 5.85， 11.7 g·kg-1）， and an estazolam （0.21 mg·kg-1） group. Insomnia model was established on days 1 to 3. p-Chlorophenylalanine （PCPA） was injected intraperitoneally at a dose of 400 mg·kg-1 into mice of the model group and administration groups for 3 consecutive days. Then， the classic depression model was established with chronic unpredictable mild stress （CUMS） for 28 consecutive days. Administration and modeling were performed simultaneously. After gavage， 24 h spontaneous activity test was performed to test sleep state， and sugar preference test and open field test were performed to evaluate anxiety-like state. The morphological changes of the hypothalamus were observed by hematoxylin-eosin （HE） staining， and the number of Nissl bodies was observed by Nissl staining. The ultrastructure of mitochondria was observed by transmission electron microscopy. The mitochondrial membrane potential assay kit （JC-1） was used to examine the mitochondrial function， and a biochemical assay kit was used to measure the ATP content in the hypothalamus. The level of reactive oxygen species （ROS） was determined by the immunofluorescence assay， and the serum levels of 5-hydroxytryptamine （5-HT）， noradrenalin （NE）， and cortisol （CORT） were determined by enzyme-linked immunosorbent assay （ELISA）. Western blot and Real-time quantitative polymerase chain reaction （Real-time PCR） were employed to determine the expression of PINK1， Parkin， microtubule-associated protein 1 light chain 3 （LC3）， and isolator protein 1 （p62） at protein and mRNA levels， respectively.ResultsThe 24-h spontaneous activity test showed that compared with the normal group， the model group did not exhibit circadian rhythm characteristics in their spontaneous activity time， while the circadian rhythm characteristics were restored in each treatment group （P<0.05）. The sucrose preference test indicated that compared with that in the normal group， the sucrose preference rate in the model group reduced （P<0.01）， and compared with that in the model group， the sucrose preference rate in each treatment group increased （P<0.01）. The open field test revealed that compared with the normal group， the model group exhibited decreased movement distance， average speed， frequency of visits to the central area， and time spent in the central area （P<0.01）， and compared with those in the model group， these parameters in each treatment group increased （P<0.05， P<0.01）. HE staining showed that compared with the normal group， the model group exhibited disarrangement of neurons in the hypothalamus， enlarged intercellular space， and severe nuclear condensation， while the degree of hypothalamic neuronal damage in each treatment group was alleviated. Nissl staining indicated that compared with the normal group， the model group demonstrated aggravated neuronal damage and increased damaged cells （P<0.01）. Compared with that in the model group， the number of damaged cells in each treatment group decreased （P<0.01）. Transmission electron microscopy showed that compared with the normal group， the model group exhibited mitochondrial swelling and rupture in the hypothalamus， with visible autophagic lysosomes in the cytoplasm. Compared with those in the model group， only a few autophagic lysosomes were observed in the BZ-L group， and the degree of mitochondrial swelling and rupture was alleviated in the other treatment groups. ROS immunofluorescence assay showed that compared with the normal group， the model group displayed enhanced red fluorescence intensity of mitochondrial ROS （P<0.01）， which was attenuated in each treatment group （P<0.01）. Mitochondrial membrane potential assay showed that compared with the normal group， the model group had declined mitochondrial membrane potential （P<0.01）， which was recovered in each treatment group （P<0.05， P<0.01）. The biochemical assay of ATP levels indicated that compared with the normal group， the model group exhibited decreased ATP content （P<0.01）， which rebound in each treatment group （P<0.05， P<0.01）. ELISA showed that compared with the normal group， the model group exhibited decreased 5-HT content and increased NE and CORT content （P<0.01）. Compared with the model group， each treatment group showed increased 5-HT content （P<0.01） and reduced NE content （P<0.01） and CORT content （P<0.05， P<0.01）. Western blot of the hypothalamus showed that compared with the normal group， the model group exhibited downregulated protein levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated protein level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated protein levels of PINK1， Parkin， and LC3 （P<0.05， P<0.01） and downregulated protein level of p62 （P<0.05， P<0.01）. Real-time PCR showed that compared with the normal group， the model group exhibited downregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated mRNA level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and downregulated mRNA level of p62 （P<0.01）.ConclusionBZ can ameliorate the insomnia and anxiety state of mice by regulating PINK1/Parkin signaling pathway to improve the mitochondrial function， enhance mitochondrial autophagy， protect neurons， and repair damaged nerve cells.Keywords：insomnia;depression;Banxia Shumitang;Zhizichi Tang;PINK1/Parkin signaling pathway;mitochondrial autophagy27|6|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
Mechanisms of Babaodan in Attenuating Acetaminophen-induced Acute Liver Injury via Metabolic Reprogramming and Inflammatory Pathways AI Introduction
Abstract：ObjectiveTo investigate the effects and potential mechanisms of Babaodan （BBD） against acetaminophen （APAP）-induced acute liver injury （ALI） based on transcriptomics.MethodsA total of 36 male C57BL/6 mice were randomly divided into 6 groups （n=6 per group）： normal group， model group， N-acetylcysteine group （NAC， 120 mg·kg-1）， and BBD low-， medium-， and high-dose groups （BBD-L， BBD-M， BBD-H groups， 75， 150， 300 mg·kg-1， respectively）. Except for the normal group， all other groups were subjected to APAP-induced ALI. The serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C） were measured in each group. Hepatic levels or activities of malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） were detected using commercial kits. Hematoxylin-eosin （HE） staining was performed to evaluate the degree of liver histopathological damage. Transcriptomic analysis was employed to screen differentially expressed genes （DEGs）， and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed to identify differential pathways involved in BBD intervention against ALI. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were applied to validate the expression of differential genes and related pathway proteins. Additionally， glucose （GLU） consumption， as well as lactate （LD） and adenosine triphosphate （ATP） content were assessed across all mouse groups.ResultsPharmacodynamic evaluation showed that， compared with the normal group， the model group exhibited significantly elevated serum levels of ALT， AST， TC， TG， and LDL-C （P<0.01）， significantly increased MDA level （P<0.01）， and significantly decreased GSH-Px level （P<0.05）. Compared with the model group， BBD intervention at different doses significantly reduced the serum levels of ALT， AST， TC， TG， and LDL-C （P<0.05， P<0.01）， increased GSH-Px level （P<0.05， P<0.01）， significantly decreased MDA level （P<0.01）， and ameliorated hepatic histopathological injury. Liver transcriptomic analysis revealed that， following high-dose BBD intervention， the core genes were mainly enriched in pathways related to inflammatory responses and energy metabolic reprogramming， including the interleukin-17 （IL-17） signaling pathway， the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， fructose and mannose metabolism， and glycolysis. Real-time PCR validation demonstrated that， compared with the normal group， the mRNA expression levels of glycolysis-related genes ［hexokinase 1 （HK1）， hexokinase 2 （HK2）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 4 （PFKFB4）， pyruvate kinase M （PKM）， and lactate dehydrogenase A （LDHA）］， as well as inflammatory cytokines ［tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）］ were significantly upregulated in the model group （P<0.05， P<0.01）. Compared with the model group， the BBD-H group showed significantly decreased mRNA expression of HK1， HK2， PFKFB3， PFKFB4， PKM， LDHA， TNF-α， IL-6， and IL-1β （P<0.05， P<0.01）. Western blot results indicated that， compared with the normal group， the model group had significantly increased expression of glycolysis-related proteins ［glucose transporter 1 （GLUT1）， HK1， PFKFB3， and PKM］， inflammatory proteins ［interleukin-18 （IL-18）， TNF-α， and IL-1β］， and phosphorylated （p）-PI3K and p-Akt proteins （P<0.05， P<0.01）. Compared with the model group， the BBD-H group exhibited significantly decreased expression of GLUT1， HK1， PFKFB3， PKM， IL-18， TNF-α， IL-1β， p-PI3K， and p-Akt （P<0.05， P<0.01）. Metabolic indicator measurements showed that， compared with the model group， the BBD-H group showed significantly reduced GLU consumption， LD and ATP content （P<0.05， P<0.01）.ConclusionBBD may alleviate APAP-induced ALI through dual regulation of metabolic reprogramming and inflammatory responses， potentially via inhibition of the PI3K-Akt signaling pathway.Keywords：Babaodan;acute liver injury;transcriptomics;metabolic reprogramming;inflammatory responses17|11|0<HTML><H-PDF><L-PDF>Updated：2026-08-31Treatment of Cardiac Aging Based on Essence-Qi-spirit Theory of Qi-collateral Doctrine AI Introduction
Abstract：Cardiac aging is a key factor in the onset and progression of cardiovascular diseases. Investigating the traditional Chinese medicine （TCM） pathogenesis and therapeutic principles of cardiac aging is of great importance for curbing the common phenomenon of the heart aging faster than the body and implementing the national strategy in response to population aging. Essence （Jing）， Qi， and spirit （Shen） are the origin， driving force， and manifestation of life， respectively. The Essence-Qi-spirit theory within the Qi-collateral doctrine delineates the core pathogenesis and therapeutic principles of aging. This framework identifies kidney essence deficiency as the fundamental cause of aging， with primordial Qi depletion as a key factor and the consumption of body and spirit as its manifestations. Corresponding treatment principles involve tonifying the kidney to replenish essence， warming and supporting primordial Qi， and nourishing the body and spirit. During the process of tonifying the kidney， regulating Yin and Yang remains essential. Relevant studies indicate that this theoretical system provides significant guidance for anti-aging research in TCM. Guided by the Essence-Qi-spirit theory within the Qi-collateral doctrine， this paper posits that kidney essence constitutes the material foundation for cardiac development， and primordial qi acts as the fundamental driver of cardiac function. Physical form and spirit together provide the structural carrier and functional manifestation of the heart. We further propose the core pathogenesis and therapeutic principles for cardiac aging. The fundamental pathogenesis lies in the deficiency and decline of kidney essence， leading to malnourishment of the heart. The key pathogenesis is the deficiency of primordial Qi， resulting in obstruction of the heart collateral. The manifestation involves the accumulation in the collateral and the dysfunction of the heart spirit. The corresponding treatment principles are tonifying the kidney and replenishing essence to nourish the heart， warming and reinforcing primordial Qi to unblock the heart collateral， and fortifying the physical form to invigorate the spirit mechanism. Existing studies demonstrate that Bazi Bushen Capsules， with the effects of tonifying the kidney， replenishing essence， warming primordial Qi， and fortifying the physical form and spirit， can delay cardiac aging. Guided by the Essence-Qi-spirit theory within the Qi-collateral doctrine， these findings support the development of effective herbal formulas to intervene in cardiac aging.Keywords：Qi-collateral doctrine;essence-Qi-spirit theory;Bazi Bushen capsules;cardiac aging17|8|0<HTML><H-PDF><L-PDF>Updated：2026-08-31Traditional Chinese Medicine Regulates Microglia-neuron Interaction to Treat Diabetes Mellitus Complicated with Depression： A Review AI Introduction
Abstract：The co-occurrence of diabetes mellitus complicated with depression （DD） is a clinically prevalent comorbidity characterized by complex pathogenesis and challenging therapeutic management， severely impairing patients' quality of life. Recent research indicates that dysregulation in microglia-neuron interaction plays a pivotal role in the pathological progression of DD. Sustained hyperglycemia can activate central microglia， promoting the activation of NOD-like receptor protein 3（NLRP3） inflammasome and the release of abundant pro-inflammatory cytokines， such as interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）， which trigger neuroinflammation. This cascade leads to hippocampal neuronal damage， impaired synaptic plasticity， and neurotransmitter imbalances， ultimately exacerbating depressive-like behaviors. Traditional Chinese medicine （TCM） offers advantages in preventing and treating DD through its multi-component， multi-target， and holistic regulatory approach. TCM can intervene in excessive microglial activation and their aberrant interactions with neurons by modulating neurotrophic signaling pathways such as brain-derived neurotrophic factor （BDNF）/tyrosine receptor kinase B （TrkB）， suppressing neuroinflammation， preserving neuronal structure and function， regulating synaptic plasticity， and improving glucose and lipid metabolism， thereby exerting synergistic therapeutic effects. Focusing on the role of microglia-neuron interaction in the pathological progression of DD， this review systematically elaborates on the research progress of TCM in regulating this interactive process， providing new perspectives and potential targets for the clinical prevention and treatment of DD.Keywords：diabetes mellitus complicated with depression;microglia;neuron;traditional Chinese medicine;mechanism14|12|0<HTML><H-PDF><L-PDF>Updated：2026-08-31- Abstract：ObjectiveTo observe the clinical efficacy and safety of Zhinao capsules in the treatment of mild and moderate sleep disorders in Alzheimer's disease patients with the syndrome of spleen-kidney deficiency and combined phlegm and stasis.MethodsA randomized， double-blind， placebo， controlled clinical trial design was adopted， and 60 Alzheimer's disease patients aged 50-85 years with mild and moderate sleep disorders due to spleen-kidney deficiency and combined phlegm and stasis were included. According to the randomized numble table method， the patients were assigned into a treatment group and a control group （30 in each group， with 29 patients in the treatment group and 28 patients in the control group finally completing the trial）. The treatment group was treated with donepezil hydrochloride tablets combined with Zhinao capsules， and the control group was treated with donepezil hydrochloride tablets combined with the simulant of Zhinao capsules for 12 weeks. The Pittsburgh Sleep Quality Index （PSQI）， smart bracelet sleep monitoring， Epworth Sleeping Scale （ESS）， Mini-Mental State Examination （MMSE）， Activities of Daily Living （ADL）， and traditional Chinese medicine symptoms were scored. Furthermore， the brain-derived neurotrophic factor （BDNF） and gamma-aminobutyric acid （GABA） levels were measured.ResultsAfter 12 weeks of treatment， the total response rate of clinical efficacy assessment in the treatment group reached 89.7%， which was significantly higher than that （21.4%） in the control group （Z=-5.14， P<0.01）. After treatment， the TCM symptom scores declined in both groups （P<0.01）， and the scores in the treatment group were lower than those in the control group （P<0.01）. After treatment， the treatment group showed decreased total score and seven component scores of the PSQI scale （P<0.05， P<0.01）， and the scores in the treatment group were lower than those in the control group （P<0.05， P<0.01）. After treatment， the treatment group showed increases in the duration of deep sleep， light sleep， rapid eye movement sleep， and total sleep at night and decreases in the time to fall asleep， the number of awakenings from sleep at night， and the time for sporadic daytime naps （P<0.01）. The control group did not show significant changes in the duration of light sleep， time to fall asleep， and number of awakenings from sleep at night. Moreover， the treatment group outperformed the control group in terms of the indicators above （P<0.05， P<0.01）. After treatment， the treatment group showed decreased scores of ESS， ADL and its subscales Physical Self-Maintenance Scale （PSMS）， and Instrumental Activities of Daily Living Scale （IADLs） and increased score of MMSE and levels of BDNF and GABA （P<0.05， P<0.01）. There was no significant difference in PSMS between the two groups， and the treatment group was significantly better than the control group in terms of the rest of the above indicators （P<0.05， P<0.01）. Patients in neither groups complained of uncomfortable symptoms.ConclusionZhinao capsules have significant clinical efficacy in treating patients with mild and moderate sleep disorders in Alzheimer’s disease patients with the syndrome of spleen-kidney deficiency and combined phlegm and stasis. Zhinao capsules can significantly reduce PSQI， ESS， and ADL scores， increase the MMSE score and the expression of BDNF and GABA， effectively optimize the structure of sleep， improve the intelligence， and enhance the ability of daily life， without causing uncomfortable symptoms. The mechanism may be related to the increase in the expression of sleep/wake-related neurotransmitters.Keywords：mild and moderate sleep disorders in Alzheimer's disease;syndrome of spleen-kidney deficiency and combined phlegm and stasis;Zhinao capsules23|6|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
Clinical Application of Qili Qiangxin Capsules in Prevention and Treatment of Chronic Heart Failure： A Review AI Introduction
Abstract：This study systematically dissects the core pathogenesis of chronic heart failure （CHF） featured by internal deficiency and external excess，imbalance of Qi，blood，Yin，and Yang，and intermingling of phlegm，blood stasis，and fluid retention. According to the traditional Chinese medicine （TCM） therapeutic principles of simultaneously treating root cause and symptoms，regulating Yin and Yang，replenishing Qi and activating blood，and promoting urination to relieve edema，this article deeply explores the formula-syndrome correspondence of Qili Qiangxin （QLQX） capsules in the treatment of CHF，providing a solid theoretical basis for the multi-effect characteristics of this drug. CHF is a common critical cardiovascular disease in clinical practice，and its pathological process involves multiple links including myocardial injury，neurohumoral disturbance，and ventricular remodeling. Its TCM pathogenesis is complex and involves multiple Zang-Fu organs，making it difficult for a single therapeutic method to achieve comprehensive coverage. QLQX capsules，formulated based on classical TCM theory，perfectly matches the pathogenic characteristics of CHF. Modern pharmacological studies have confirmed that QLQX capsules possess definite cardiotonic，diuretic，and vasodilatory effects. The active ingredients of QLQX capsules can rapidly and effectively alleviate the core clinical symptoms such as chest tightness，shortness of breath，decreased exercise tolerance，limb edema，palpitations，and fatigue of CHF patients by enhancing myocardial contractility and coronary blood flow，improving renal water excretion function，dilating peripheral blood vessels，and reducing cardiac load，thereby significantly improving patients' quality of life. On the basis of analyzing the symptomatic treatment of CHF with QLQX capsules，this study further expounds that the drug can intervene in ventricular remodeling through multiple pathways and targets，regulate the pathological mechanism of CHF，improve vascular endothelial function，mediate the activation of related signaling pathways，inhibit the transdifferentiation of cardiac fibroblasts，and regulate myocardial energy metabolism，thus delaying disease progression. QLQX capsules exert significant benefits in reducing composite cardiac events，improving New York Heart Association （NYHA） cardiac function classification，left ventricular ejection fraction （LVEF），6-minute walking distance （6MWD），and quality of life，demonstrating favorable clinical value. With the TCM pathogenesis of CHF as the guiding principle and modern pharmacology as the evidence，this study systematically clarifies the core advantage of QLQX capsules in treatment based on syndrome differentiation and multi-target synergy through the in-depth integration of TCM theory and modern pharmacology. It provides academic support with both theoretical depth and practical value for TCM intervention in CHF，and contributes TCM wisdom and schemes to the construction of a chronic disease management system with Chinese characteristics.Keywords：Qili Qiangxin capsules;chronic heart failure;cardioprotective effect;traditional Chinese medicine28|9|0<HTML><H-PDF><L-PDF>Updated：2026-08-31Real-World Cohort Study of Qingre Huoxue Prescription for Treating Rheumatoid Arthritis Complicated by Hyperhomocysteinemia AI Introduction
Abstract：ObjectiveTo evaluate the effects of Qingre Huoxue prescription combined with methotrexate （MTX） and folic acid （FA） on homocysteine （Hcy） levels and disease activity in patients with rheumatoid arthritis （RA） complicated by hyperhomocysteinemia （HHcy）.MethodsOn the basis of a multicenter real-world cohort from the China Registry of Traditional Chinese Medicine for Rheumatism （CERTAIN） platform，408 patients with RA complicated by HHcy were selected and included in this study. Treatment with Qingre Huoxue prescription was used as the exposure factor. According to whether Qingre Huoxue prescription was combined with MTX and FA，patients were assigned into an exposure group of 281 cases and a control group of 127 cases. Follow-ups were conducted every three months，with the primary outcome indicator being the achievement rate of target Hcy level. A generalized estimating equation model was adopted to analyze the dynamic changes in Hcy level under different medication regimens. Kaplan-Meier analysis was performed to evaluate the cumulative achievement rate of target Hcy level in the two groups，and Cox regression analysis was conducted to explore the predictive factors affecting the achievement rate of target Hcy level. Changes in erythrocyte sedimentation rate （ESR），C-reactive protein （CRP），28-joint Disease Activity Score （DAS 28），and Health Assessment Questionnaire-Disability Index （HAQ-DI） scores before and after the first combined treatment with Qingre Huoxue prescription were compared between the two groups.ResultsThe Hcy level in the exposure group showed a gradual decreasing trend over time，while the decrease in Hcy level was not significant in the control group. At the 12-month follow-up，the achievement rate of target Hcy level in the exposure group （124/281，44.13%） was higher than that in the control group （23/127，18.11%，P<0.01）. Multivariable Cox regression analysis showed that treatment with Qingre Huoxue Decoction （hazard ratio（HR）= 3.013，95% confidence interval （CI） 2.188-4.149， P<0.001）， absence of comorbidities （HR=2.035， 95%CI 1.352-3.061， P<0.001）， and baseline Hcy <15 μmol·L-1 （HR=1.810， 95%CI 1.390-2.357， P<0.001） were significantly associated with an increased likelihood of achieving target Hcy levels within 6 months. In contrast， higher PGA scores were associated with a reduced likelihood of achieving target Hcy levels （HR=0.991， 95% CI 0.986-0.997， P=0.003）. After treatment，the exposure group demonstrated reductions in ESR，CRP，and DAS 28 scores （P<0.05） and had lower ESR，CRP and DAS 28 scores than the control group （P<0.05）.ConclusionEven after taking FA supplements，some RA patients undergoing MTX treatment still have high Hcy levels. When being used in conjunction with MTX and FA，Qingre Huoxue prescription can effectively lower the Hcy level and disease activity in RA patients with HHcy，outperforming Western treatment alone.Keywords：rheumatoid arthritis;hyperhomocysteinemia;Qingre Huoxue prescription;achievement rate of target homocysteine level;real-world cohort study22|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31- Abstract：ObjectiveTo observe the effect of modified Huanglian Wendantang on oxidative stress in metabolic syndrome.MethodsA total of 180 patients with metabolic syndrome treated in the outpatient clinics and wards of the First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine from October 2023 to May 2025 were enrolled in this study. According to the randomized numerical table method， the patients were assigned into two groups （90 cases）. The basic treatment of the two groups was the same， and the observation group was additionally treated with modified Huanglian Wendantang. The course of treatment was 3 months. The two groups were compared in terms of traditional Chinese medicine （TCM） efficacy， obesity degree ［waist circumference （WC）， body mass index （BMI）， waist-to-hip ratio （WHR）， waist-to-height ratio （WHtR）］， blood pressure indicators ［systolic blood pressure （SBP） and diastolic blood pressure （DBP）］， lipids and glucose indicators ［total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein cholesterol （HDL-C）， low-density lipoprotein cholesterol （LDL-C）， fasting insulin （FINS）， fasting glucose （FPG）， 2-hour postprandial glucose （2 h PG）， and glycosylated hemoglobin （HbA1c）］， insulin resistance indicators ［homeostatic model assessment for insulin resistance （HOMA-IR）， triglyceride-glucose index （TYG index）， triacylglycerol-to-high-density lipoprotein cholesterol （TG/HDL） ratio］， oxidative stress indicators ［malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione （GSH）， glutathione peroxidase （GSH-Px）， catalase （CAT）， and reactive oxygen species （ROS）］， and the safety of treatment.ResultsIn terms of TCM efficacy， the treatment in the observation group was significantly effective in 46 cases， effective in 30 cases， and ineffective in 10 cases， with the total effective rate of 88.4%. The treatment in the control group was significantly effective in 33 cases， effective in 28 cases， and ineffective in 23 cases， with the total effective rate of 72.6%. The observation group had higher total effective rate than the control group （χ2=11.26，P<0.05）. After treatment， both groups showed declined levels of WC， BMI， WHR， WHtR， SBP， DBP， TC， TG， LDL-C， FPG， FINS， 2 h PG， HbA1c， HOMA-IR， TG/HDL ratio， TYG index， MDA， and ROS and elevated levels of HDL-C， SOD， GSH， GSH-Px， and CAT （P<0.05）. After treatment， the observation group showed lower levels of WC， BMI， WHR， WHtR， TC， TG， LDL-C， FPG， FINS， 2 h PG， HbA1c， HOMA-IR， TG/HDL ratio， TYG index， MDA， and ROS and higher levels of HDL-C， SOD， GSH， GSH-Px， and CAT than the control group （P<0.05）. However， after treatment， there was no significant difference in SBP or DBP between the observation group and the control group. No significant adverse reactions were observed in either group.ConclusionModified Huanglian Wendantang can significantly alleviate metabolic syndrome symptoms and reduce oxidative stress， exhibiting antioxidant effects. Moreover， it does not induce adverse reactions， demonstrating safety.Keywords：metabolic syndrome;modified Huanglian Wendantang;oxidative stress18|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
Traditional Chinese Medicine Intervenes in Endoplasmic Reticulum Stress to Treat Diabetic Microvascular Complications：A Review AI Introduction
Abstract：Diabetic microvascular complications （DMC） are major chronic complications of diabetes，primarily including diabetic kidney disease （DKD），diabetic retinopathy （DR），diabetic cardiomyopathy （DCM），and diabetic peripheral neuropathy （DPN）. These complications significantly impact patients’ quality of life and prognosis. Modern medicine primarily focuses on symptomatic control in the treatment of DMC，with limited ability to reverse the disease progression. Endoplasmic reticulum stress （ERS），as a central event under hyperglycemic toxicity，is not only a key cause of pancreatic β-cell dysfunction （reduced insulin synthesis and secretion） but also a core driver of damage in various target organs of DMC. It activates three signaling pathways of the unfolded protein response （UPR）—inositol-requiring enzyme 1 （IRE1），activating transcription factor 6 （ATF6），and protein kinase R-like endoplasmic reticulum kinase （PERK），intertwining processes such as autophagy，apoptosis，oxidative stress，and calcium homeostasis imbalance. Traditional Chinese medicine （TCM） offers multi-target and multi-pathway therapeutic advantages and can curb the pathological progression of DMC by regulating ERS. This article systematically reviews the relationships of ERS with pancreatic β-cell function，insulin synthesis，and insulin secretion，and elucidates the core signaling pathways through which ERS mediates DMC. Furthermore，it categorizes and summarizes experimental evidence and mechanisms of single medicinal herbs and their extracts，TCM compound formulas，and modern TCM preparations in regulating ERS for the treatment of various DMC subtypes. Finally，this article proposes ERS as a molecular bridge for integrating traditional Chinese and Western medicine in DMC treatment. Future research should leverage emerging technologies such as network pharmacology，multi-omics analysis，and nano-formulations to establish a synergistic network combining modern hypoglycemic drugs and TCM regulation of ERS. This approach is expected to achieve dual efficacy，enhance drug targeting and bioavailability，deepen the understanding of scientific connotation of TCM，and pave new avenues for the prevention and treatment of DMC.Keywords：diabetic microvascular complications;endoplasmic reticulum stress （ERS）;apoptosis;autophagy;traditional Chinese medicine12|8|0<HTML><H-PDF><L-PDF>Updated：2026-08-31- Abstract：ObjectiveTo investigate the mechanisms of Zuojinwan in the treatment of colorectal cancer from the perspective of inhibiting M2 polarization of tumor-associated macrophages.MethodsA colorectal cancer mouse model was established by azoxymethane （AOM）/dextran sulfate sodium （DSS）. Body weight was recorded， disease activity index （DAI） and tumor number were calculated， and hematoxylin-eosin （HE） staining was used to observe colonic pathological changes. Enzyme-linked immunosorbent assay （ELISA） was used to detect the levels of interleukin-6 （IL-6）， transforming growth factor-β （TGF-β）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in colonic homogenates. Immunohistochemistry was used to detect proliferating cell nuclear antigen （PCNA） expression in the colon， and immunofluorescence was used to detect mannose receptor （CD206） expression in macrophages. In vitro， M2 macrophages were induced using IL-4/IL-13， and macrophages were treated with different concentrations of Zuojinwan-containing serum. CD206 and differentiation cluster 86 （CD86） were analyzed by flow cytometry. A CT26 and RAW264.7 macrophage co-culture system was established， and the migration and proliferation abilities of CT26 cells were detected using Transwell assays and trypan blue exclusion. Finally， proteomics was used to screen key proteins and signaling pathways involved in Zuojinwan-mediated inhibition of M2 polarization of tumor-associated macrophages in colorectal cancer， and Western blot was used for validation.ResultsIn animal experiments， compared with the blank group， mice in the model group showed significantly decreased body weight （P<0.01）， significantly increased DAI scores （P<0.01）， and significantly increased tumor number （P<0.01）， with severe colonic carcinogenesis and lymphatic metastasis. The protein expression levels of PCNA and CD206 were significantly increased （P<0.01）， and the levels of IL-6， IL-1β， TNF-α， and TGF-β in colonic homogenates were significantly increased （P<0.01）. Compared with the model group， mice in the Zuojinwan intervention group showed significantly higher body weight （P<0.05）， significantly decreased DAI scores （P<0.01）， and significantly reduced tumor numbers （P<0.01）. The protein levels of PCNA and CD206 were significantly decreased （P<0.05）， and the levels of IL-6， IL-1β， TNF-α， and TGF-β in colonic homogenates were significantly decreased （P<0.05）. In the CT26 and RAW264.7 co-culture system in vitro， compared with the blank group， co-culture with M2-type RAW264.7 macrophages significantly increased CT26 cell migration rate and proliferation number （P<0.01）. Compared with the M2 group （M2-type macrophages）， the proportion of CD86 was significantly increased in the Zuojinwan-containing serum group （P<0.01）， while the CT26 cell migration rate and proliferation number were significantly decreased in the 8% Zuojinwan-containing serum group （P<0.01）. Proteomics analysis indicated that tumor necrosis factor-α-induced protein 8-like protein 1 （TIPE1） may be a key target through which Zuojinwan regulates macrophage phenotypic transformation to inhibit colorectal cancer. The phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway showed the highest enrichment. Compared with the blank group， the levels of TIPE1， p-PI3K， and p-Akt in M2 macrophages were significantly increased （P<0.05，P<0.01）. After treatment with Zuojinwan-containing serum， the levels of TIPE1， p-PI3K， and p-Akt were significantly decreased （P<0.05，P<0.01）.ConclusionZuojinwan may inhibit colorectal cancer proliferation and migration by suppressing M2 polarization of tumor-associated macrophages， which may be associated with inhibition of the PI3K/Akt signaling pathway in tumor-associated macrophages.Keywords：Zuojinwan;formula;colorectal cancer;tumor-associated macrophages;tumor necrosis factor-α-induced protein 8-like protein 1 （TIPE1）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）signaling pathway12|6|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
- Abstract：ObjectiveTo observe how Banxia Xiexintang affects programmed cell death 1 ligand 1 （PD-L1） expression induced by exosomes derived from gastric cancer cells in bone marrow mesenchymal stem cells （BMSCs） through the protein kinase B （Akt）/c-myelocytomatosis oncogene （c-Myc） signaling axis， and its effects on the migration of BMSCs and gastric cancer cells.MethodsExosomes were isolated from human gastric cancer NCI-N87 cells and identified by transmission electron microscopy and Western blot. Rat BMSCs were passaged and identified by immunofluorescence staining. A Transwell chamber was used to create a non-contact co-culture system for NCI-N87 exosomes and BMSCs. The experiment was designed with normal， model， Banxia Xiexintang （10% serum containing Banxia Xiexintang）， PD-L1 monoclonal antibody （10% blank serum containing PD-L1 antibody）， and combination （10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody） groups. The suspension of BMSCs was added to the upper chamber of each group， with the normal group receiving serum culture medium without exosomes in the lower chamber， and the model group receiving NCI-N87 exosomes. The Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group received 10% serum containing Banxia Xiexintang， 10% blank serum containing PD-L1 monoclonal antibody， and 10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody， respectively， in the upper chamber. After 96 h， BMSCs from the upper chamber were collected， and the protein levels of p-Akt， Akt， c-Myc， and PD-L1， as well as the mRNA levels of Akt， c-Myc， and PD-L1， were determined by Western blot and Real-time PCR， respectively. The migration of BMSCs and NCI-N87 was assessed by the Transwell method.ResultsCompared with the normal group， the model group showed increases in protein levels of p-Akt， c-Myc， and PD-L1， as well as mRNA levels of c-Myc and PD-L1 （P<0.05， P<0.01）， and no significant change in the protein and mRNA levels of Akt. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in protein levels of p-Akt， c-Myc， and PD-L1 （P<0.01）. In addition， they had significant effects on the protein and mRNA levels of Akt. The combination group showed greater reductions in the protein and mRNA levels of c-Myc and PD-L1 than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.05）. Compared with the normal group， the model group showed increases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）， with the combination group showing greater reductions in the number of migrating NCI-N87 and BMSCs than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.01）.ConclusionBanxia Xiexintang can lower the PD-L1 expression induced by gastric cancer cell-derived exosomes in BMSCs induced and inhibit the migration of BMSCs and gastric cancer cells. Moreover， it has a synergistic effect when being used together with PD-L1， possibly related to the regulation of the Akt/c-Myc signaling axis.Keywords：Banxia Xiexintang;gastric cancer cell-derived exosomes;bone marrow mesenchymal stem cells;protein kinase B （Akt）/c-mycmyelocytomatosis oncogene （c-Myc） signaling axis;programmed cell death 1-ligand 1 （PD-L1）22|7|0<HTML><H-PDF><L-PDF>Updated：2026-08-31
