Chinese Medicine最新文献

{"title":"Acupuncture promotes muscle cells ATP metabolism in ST36 acupoint local exerting effect by activating TRPV1/CaMKII/AMPK/PGC1α signaling pathway.","authors":"Zhihan Chen, Kaifang Yao, Xinrui Wang, Yangyang Liu, Simin Du, Shenjun Wang, Yuxin Fang, Yuan Xu, Zhifang Xu, Xiaowei Lin, Yi Guo","doi":"10.1186/s13020-025-01169-z","DOIUrl":"10.1186/s13020-025-01169-z","url":null,"abstract":"<p><p>At present, a number of studies have shown that acupuncture at Zusanli (ST 36) can relieve pain, but the changes of local microenvironment in the acupoint area after acupuncture have not been elucidated. As a temperature and pain receptor, TRPV1 plays an important role in pain perception and inflammation regulation. In this study, RT-PCR technique was used to screen the types of mechanically sensitive ion channels in the local response to acupuncture in the acupoint area, and western bolt technique was used to verify in gene knockout and antagonist injection mice. Immunofluorescence double labeling technique was used to further determine the key cell types of TRPV1-mediated acupuncture analgesia. Finally, through the combined analysis of proteomics and phosphorylated proteomics, the local signaling pathways of acupoints that can be activated by acupuncture were analyzed. This study systematically explored the analgesic effect of acupuncture on inflammatory pain in mice and its mechanism. The study found that acupuncture can significantly improve the thermal pain threshold and mechanical pain threshold in mice, showing a significant analgesic effect. Further analysis revealed that this analgesic effect was closely related to the up-regulation of local TRPV1 expression at ST36, and its deletion or functional inhibition would significantly weaken the analgesic effect of acupuncture. In addition, we also found that acupuncture in the deep muscle layer can more effectively promote the expression and activity of TRPV1 than in the superficial fascia layer, and muscle cells are the key cell types of TRPV1-mediated acupuncture analgesia. Finally, through the combined analysis of multi-omics, it was clear that acupuncture could activate the local signal pathway TRPV1/CaMKII/AMPK/PGC1α to exert analgesic effect. In conclusion, this study not only confirmed the analgesic effect of acupuncture on inflammatory pain in mice, but also revealed the core role of TRPV1 in the mechanism of acupuncture analgesia, especially the important contribution of TRPV1 expression and activity in the muscle layer of ST36 acupoint to the analgesic effect of acupuncture, which provided a new scientific basis and potential therapeutic target for acupuncture treatment of inflammatory pain.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"112"},"PeriodicalIF":5.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12257683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ganoderma lucidum spore oil alleviates psychological stress-evoked tumor progression by enhancing FcγR-mediated macrophage phagocytosis.","authors":"Dong-Dong Li, Zi-Xuan Li, Yang-Fan Zhou, Ling Jin, Wan-Li Liang, Wen-Dong Xu, Xiang Luo, Guan-Di Xiao, Qi-Jun Chen, Ting Xie, Hui Xu, Yang Liu, Hong-Fei Cai, Yun-Feng Cao, Wan-Yang Sun, Yi-Fang Li, Lei Liang, Ju-Yan Liu, Yan-Ping Wu, Rong-Rong He","doi":"10.1186/s13020-025-01168-0","DOIUrl":"10.1186/s13020-025-01168-0","url":null,"abstract":"<p><strong>Background: </strong>Ganoderma lucidum (G. lucidum), has been documented as a medicinal herb in classical texts and officially recognized in both Eastern and Western pharmacopeias. G. lucidum spore oil (GLSO), a lipid substance extracted from sporoderm-broken spores, has shown potential in enhancing immune function and prolonging the survival of tumor patients. However, the mechanisms underlying GLSO's immunomodulatory effects remain poorly unknown.</p><p><strong>Methods: </strong>The effect of psychological stress on tumor progression and macrophage phagocytosis was analyzed by an in vivo small animal imaging system and flow cytometry. The effect of psychological stress on phospholipid composition in mice was investigated by LC-MS/MS based lipidomic analysis. The effectiveness of GLSO in tumor-bearing mice subjected to restraint stress was observed by tumor burden and phagocytosis of macrophages. Finally, the underlying mechanism of GLSO on macrophage phagocytosis in mice subjected to psychological stress was explored by RNA-seq, and the FcγR/SYK-mediated macrophage phagocytosis pathway was confirmed by qPCR, Western blotting, and confocal laser technology.</p><p><strong>Results: </strong>Our study discovered that psychological stress-triggered tumor progression is contributed to by liposoluble components-impaired macrophage phagocytosis. Lipidomics analysis further identified lysophosphatidylinositol [LPI (18:0)] as a key factor suppressing macrophage phagocytic capacity under psychological stress. GLSO was shown to mitigate psychological stress-evoked tumor progression by enhancing macrophage-mediated phagocytosis of tumor cells in vivo. Mechanistically, transcriptomics analysis revealed that the LPI-mediated FcγR phagocytosis pathway is a crucial axis driving the therapeutic effect of GLSO under psychological stress.</p><p><strong>Conclusion: </strong>Our findings illustrate that psychological stress-promoted cancer progression is contributed by the critical liposoluble components LPI (18:0)-mediated FcγR phagocytosis signaling inhibition. GLSO alleviates the dampened phagocytosis of macrophages caused by stress through regulating LPI/FcγR-mediated phagocytosis-related pathways, underscoring its potential as a therapeutic intervention for stress-related tumor progression.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"111"},"PeriodicalIF":5.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12257750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of solamargine in hepatic metastasis of colorectal cancer: induction of ferroptosis and elimination of cancer stem cells.","authors":"Shenglan Liu, Junhong Wu, Hao Huang, Bin Hu, Dong Xie, Fuqiang Cao, Jingxuan Li, Caiyao Guo, WeiJie Peng, Yanli Jin, Wei Dai","doi":"10.1186/s13020-025-01171-5","DOIUrl":"10.1186/s13020-025-01171-5","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is a prevalent malignant tumor globally, ranking third in incidence and second in mortality. Metastasis is the main cause of death in patients with CRC. Solanum nigrum L. (SNL), a traditional Chinese medicinal herb endowed with detoxification, blood circulation enhancement, and anti-swelling properties, has been widely used in folk prescriptions for cancer treatment in China. Solamargine (SM) is the major steroidal alkaloid glycoside purified from SNL. However, its role and mechanism against metastatic CRC are not yet clear. The purpose of this study was to evaluate the inhibitory effect of SM on human hepatic metastatic CRC and investigate its underlying mechanism.</p><p><strong>Methods: </strong>CCK-8 assay, colony-formation assay, transwell assay, flow cytometry, tumoursphere formation assay, reverse-transcription quantitative PCR (RT-qPCR), Western blotting, transcriptomic sequencing and ferroptosis analysis were performed to reveal the efficacy and the underlying mechanism of SM in CRC cell lines. In vivo, allograft model, patient-derived xenograft (PDX) model, and liver metastatic model were performed to verify the effect of SM on the growth and metastasis of CRC.</p><p><strong>Results: </strong>SM was found to suppress hepatic metastasis in CRC by effectively targeting key cellular processes, including proliferation, survival, and stemness. RNA sequencing showed that SM could induce ferroptosis, which was confirmed by elevated lipid reactive oxygen species (ROS) and downregulated glutathione peroxidase 4 (GPX4) and glutathione synthetase (GSS) in CRC cells and xenografts. Induction of ferroptosis by SM was regulated by nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, downregulation of β-catenin was found to be fundamental for the SM-enabled cancer stem cells (CSCs) elimination and metastasis blockage in CRC.</p><p><strong>Conclusion: </strong>Our results indicated that SM is a promising therapeutic drug to inhibit hepatic metastasis in CRC by inducing ferroptosis and impeding CSCs.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"110"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Juanbi Qianggu Formula inhibits fibroblast-like synovicytes activation via repressing LncRNA ITSN1-2 to promote RIP2 K48 ubiquitination.","authors":"Yanqin Bian, Fang Li, Xinyu A, Zheng Xiang, Nanshan Ma, Jianye Wang, Boran Cao, Pengfei Xin, Xuan Cheng, Chang Liu, Bei Xiang, Jun Shen, Qigui Lu, Lianbo Xiao","doi":"10.1186/s13020-025-01164-4","DOIUrl":"10.1186/s13020-025-01164-4","url":null,"abstract":"<p><strong>Background: </strong>Long non-coding RNA ITSN1-2(lncRNA ITSN1-2) promotes fibroblast-like synovicytes (FLS) proliferation and suppress apoptosis through activation of the NOD2/RIP2 signaling pathway, thereby exacerbating synovitis in Rheumatoid arthritis (RA) pathology. Juanbi Qianggu Formula (JBQG), a clinically efficacious traditional Chinese medicine, has shown significant efficiency in inhibiting FLS activation in RA and alleviating disease progression in RA patients. However, the molecular mechanism underlying JBQG's anti-arthritic effects remains incompletely understood, particularly regarding its potential to modulate lncRNA ITSN1-2-mediated NOD2/RIP2 signaling in FLS activation. This study aims to investigate the functional interplay between JBQG and the lncRNA ITSN1-2/NOD2/RIP2 axis in regulating FLS behavior during RA development.</p><p><strong>Methods: </strong>Synovial tissues were collected from 24 rheumatoid arthritis (RA) patients and 20 osteoarthritis (OA) patients to observe the lncRNA ITSN1-2/NOD2/RIP2 signal in RA synovial tissue and its correlation with RA inflammation and bone destruction. Blood-absorbed components of JBQG were analyzed through mass spectrometry, while network pharmacology and in vitro experiments were conducted to investigate JBQG's regulatory effects on NOD2/RIP2 signaling. Mechanistic studies focused on lncRNA-ITSN1-2/miR-2683-3p/PELI3/RIP2 interactions, employing dual-luciferase assays, FISH staining, and Co-IP/Western blot. To evaluate therapeutic efficacy, a collagen-induced arthritis (CIA) rat model with lncRNA ITSN1-2 overexpression was established. JBQG's effects were assessed through histopathological examination and serum inflammation factors analysis following 23 g/kg/day treatment for 4 weeks.</p><p><strong>Results: </strong>LncRNA ITSN1-2/NOD2/RIP2 signaling was significantly activated in RA synovial tissues, showing profound correlation with RA disease inflammation and progression. JBQG treatment reduced cytoplasmic lncRNA ITSN1-2 levels in FLS, thereby inhibiting NOD2/RIP2 pathway activation and FLS functions in migration and invasion. Mechanistically, lncRNA ITSN1-2 exerted competitive endogenous RNA (ceRNA) activity by sequestering miR-2683-3p, which upregulated PELI3 expression. This induction promoted RIP2 K48 ubiquitination, destabilizing RIP2 protein integrity and inhibiting downstream NF-κB signaling. Consequently, FLS migratory and invasive capacities were significantly diminished, underscoring JBQG's dual regulatory impact on lncRNA-miRNA cross-talk and inflammatory cytokine cascades.</p><p><strong>Conclusion: </strong>This study demonstrates that JBQG exerts potent anti-arthritic effects in RA therapy through dual regulatory mechanisms targeting the lncRNA ITSN1-2/miR-2683-3p/PELI3/RIP2 axis.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"109"},"PeriodicalIF":5.3,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Buyang Huanwu Decoction improves energy metabolism disorders after cerebral ischemia-reperfusion by regulating the SIRT1/AMPK signaling pathway to promote glycolysis and the tricarboxylic acid cycle.","authors":"Zhongji Hu, Nujiao Deng, Yanling Li, Yang Bai, Xiao Lan, Tingting Xiong, Huang Ding, Xiaodan Liu, Changqing Deng","doi":"10.1186/s13020-025-01163-5","DOIUrl":"10.1186/s13020-025-01163-5","url":null,"abstract":"<p><strong>Background: </strong>Buyang Huanwu Decoction (BYHWD), a traditional Chinese medicine formula for cerebral infarction, exerts neuroprotective effects by enhancing cerebral energy metabolism, yet its precise mechanisms remain elusive.</p><p><strong>Objective: </strong>To explore the effects of BYHWD on improving cerebral ischemia-reperfusion injury (CIRI) with Qi deficiency and blood stasis syndrome from an energy metabolism perspective and verify it through experiments.</p><p><strong>Methods: </strong>A rat model of CIRI with Qi deficiency and blood stasis syndrome was established and intervened with BYHWD. The therapeutic effect of BYHWD was evaluated using Longa score, Qi deficiency and blood stasis syndrome score, pathological staining, and colorimetric assays. Untargeted metabolomics was used to identify differential metabolites and regulatory mechanisms, and in vivo and in vitro models were constructed for validation.</p><p><strong>Results: </strong>BYHWD ameliorated neurological deficits and Qi deficiency and blood stasis syndrome in rats, reduced brain pathology, and increased energy substances. Untargeted metabolomics analysis suggested BYHWD enhanced cerebral energy metabolism via nicotinate and nicotinamide metabolism and AMPK signaling, involving SIRT1/AMPK regulation and promotion of glycolysis and the tricarboxylic acid (TCA) cycle. Validation experiments showed BYHWD activated the SIRT1/AMPK signaling pathway in brain tissue, promoting glucose uptake and enhancing the expression of proteins related to glycolysis, mitochondrial biogenesis, and the TCA cycle. Similar results were observed in HT22 cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R).</p><p><strong>Conclusion: </strong>BYHWD improved cerebral energy metabolic disorders by activating the SIRT1/AMPK signaling pathway, thereby enhancing glycolytic capacity and TCA cycle capacity. This study elucidated the mechanisms of BYHWD and provided a theoretical basis for its rational application.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"108"},"PeriodicalIF":5.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12232815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Herb-drug interactions in oncology: pharmacodynamic/pharmacokinetic mechanisms and risk prediction.","authors":"Xiaoyan Duan, Xiaoyu Fan, Haiyan Jiang, Jie Li, Xue Shen, Zeao Xu, Ziqi Zhou, Jia Xu, Chongze Chen, Hongtao Jin","doi":"10.1186/s13020-025-01156-4","DOIUrl":"10.1186/s13020-025-01156-4","url":null,"abstract":"<p><p>The prevalence of herbal medicines has gained widespread, particularly among cancer patients seeking adjunctive therapies. Co-administered with anticancer drugs (ACDs) frequently, herbal medicines result in increasing cases of herb-drug interactions (HDIs), following the serious clinical consequences. While herbal medicines pose negative impacts, such as limiting efficacy and increasing toxicity of ACDs, they also offer potential benefits, including enhancing bioavailability, reducing adverse reactions, and reversing tumor drug resistance. This review is the first to systematically characterize HDI molecular mechanisms at both pharmacodynamic (PD) and pharmacokinetic (PK) levels, elucidating how herbal medicines modulate ACDs efficacy and safety through antagonism/synergy/detoxification target, metabolic enzymes, and transporters. In particular, emerging risk prediction methodologies are proposed to assess the clinical occurrence of potential PD/PK-mediated HDIs. We provide a novel insight for promoting the mechanism study of HDIs, facilitating the safe and effective integration of herbal medicines into cancer treatment.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"107"},"PeriodicalIF":5.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12232703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integration bile acid metabolomics and gut microbiome to study the anti-liver fibrosis effects of total alkaloids of Corydalis saxicola Bunting.","authors":"Qianyi Wang, MeiLing Zhang, Mingwei Meng, Zhuo Luo, Ziping Pan, Lijun Deng, Jinghua Qin, Bingjian Guo, Dan Zhu, Yanmin Zhang, Hongwei Guo, Yonghong Liang, Zhiheng Su","doi":"10.1186/s13020-025-01158-2","DOIUrl":"10.1186/s13020-025-01158-2","url":null,"abstract":"<p><strong>Background: </strong>Bile acids and gut microbiota participate in the pathogenesis of liver fibrosis (LF). The total alkaloids of Corydalis saxicola Bunting (TACS) is a traditional Chinese medicine extract that has been used to treat LF, but the underlying mechanisms are not clear. This study performed integrated metabolomics and gut microbiome analysis to study the anti-LF mechanism of TACS using a rat model.</p><p><strong>Methods: </strong>Ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) was used to identify the chemical compounds in TACS. Biochemical and histopathological analysis were performed to determine the efficacy of TACS. Bile acid-targeted metabolomics was used to assess changes in the bile acid (BA) profiles in TACS-treated LF rats. 16S rRNA gene sequencing and metagenomics were used to assess changes in the gut microbiota of the TACS-treated LF rats. Antibiotic cocktail treatment and fecal microbiota transplantation (FMT) were used to determine the relationship between the gut microbiota and the anti-LF effects of TACS. Metagenomics was used to identify significantly enriched gut microbiota after TACS treatment and its correlation with the anti-LF effects was verified by in vivo experiments.</p><p><strong>Results: </strong>TACS treatment significantly reduced the levels of serum liver enzymes, fibrosis and pro-inflammatory cytokines in the liver. TACS significantly increased the levels of chenodeoxycholic acid (CDCA) and taurochenodeoxycholic acid (TCDCA) in the cecum and decreased the levels of cholic acid (CA) and deoxycholic acid (DCA) in the liver of the LF rats. TACS significantly increased the abundances of Lactobacillus and Akkermansia in the LF rats. Antibiotic cocktail treatment and FMT have shown that the effect of TACS cure liver fibrosis depends on the gut microbiota. The abundance of Lactobacillus reuteri was significantly increased by TACS. Administration of Lactobacillus reuteri via gavage ameliorated LF.</p><p><strong>Conclusions: </strong>TACS exerted anti-LF effects in rats by modulating bile acid metabolism and gut microbiome.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"106"},"PeriodicalIF":5.3,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hederasaponin C ameliorates chronic obstructive pulmonary disease pathogenesis by targeting TLR4 to inhibit NF-κB/MAPK signaling pathways.","authors":"Yujie Ning, Liting Huang, Qin-Qin Wang, Lina Liu, Xinghua Ni, Xiaoyun Xie, Jingyu Liu, Qian Su, Shilin Yang, Renyikun Yuan, Hongwei Gao","doi":"10.1186/s13020-025-01155-5","DOIUrl":"10.1186/s13020-025-01155-5","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a complex respiratory disorder characterized by persistent respiratory symptoms and progressive airflow limitation. Long-term exposure to harmful particulates and gases causes structural abnormalities in the airways and alveoli, activating NF-κB/MAPK signaling pathways that drive chronic inflammation and tissue remodeling. Key features include an imbalance between proteolytic enzymes and inhibitors mediated by matrix metalloproteinases, and excessive mucus secretion due to mucin overexpression. These factors exacerbate airway obstruction and inflammation, contributing to disease progression. Hederasaponin C (HSC), a triterpenoid saponin with anti-inflammatory properties, shows potential in mitigating COPD-related inflammation, but its precise mechanisms require further investigation.</p><p><strong>Methods: </strong>We investigated the impact of HSC on COPD models induced by CSE + LPS using a comprehensive approach. In vitro studies included Western blotting, qRT-PCR, ELISA, and immunofluorescence to assess key proteins in NF-κB/MAPK signaling pathways, MMP9 and MMP12 expression, and mucin levels (MUC-5AC, MUC-5B). Binding affinity between HSC and TLR4 was evaluated using molecular docking, SPR analysis, and CETSA. DNA methylation at MUC-5B chr11:1243469 position was detected using an Agilent 2100 Bioanalyzer. In vivo, a COPD mouse model induced by cigarette smoke and LPS (CS + LPS) was developed, and HSC treatment effects were evaluated using H&E staining, multiplex immunofluorescence staining, Western blot, and ELISA kits.</p><p><strong>Results: </strong>HSC significantly inhibited CSE + LPS-induced inflammation by targeting TLR4 and attenuating NF-κB/MAPK signaling pathways overactivation. It also downregulated MMP9, MMP12, MUC-5AC, and MUC-5B expression and suppressed MUC-5B chr11:1243469 position DNA methylation. In vivo, HSC alleviated COPD symptoms in CS + LPS-induced mice, reducing TLR4/NF-κB/MAPK signaling pathways overactivation and smoking-associated factors.</p><p><strong>Conclusion: </strong>HSC targets TLR4, attenuates NF-κB/MAPK signaling pathways overactivation, reduces MMP9, MMP12, MUC-5AC, and MUC-5B expression, and suppresses MUC-5B chr11:1243469 position DNA methylation. These actions reduce inflammation, restore protease-antiprotease balance, and mitigate excessive mucus secretion, highlighting the promise of HSC as a viable treatment strategy for COPD management.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"104"},"PeriodicalIF":5.3,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12225042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating network pharmacology and multi-omics in a systems approach: a mechanism study of Jinhong tablets against chronic superficial gastritis.","authors":"Lihao Xiao, Tingyu Zhang, Yun Liu, Chayanis Sutcharitchan, Qingyuan Liu, Xiaoxue Fan, Jian Feng, Huifang Gao, Shao Li, Tong Zhang","doi":"10.1186/s13020-025-01138-6","DOIUrl":"10.1186/s13020-025-01138-6","url":null,"abstract":"<p><strong>Background: </strong>Chronic gastritis (CG) significantly impacts patients' quality of life and can progress to more severe gastric conditions. In China, Traditional Chinese Medicine (TCM) has been widely applied for its holistic efficacy in treating chronic superficial gastritis (CSG), including formulas like Jinhong Tablets (JHT), known for their anti-inflammatory effects. However, the mechanism of action of JHT in treating CSG still requires further clarification.</p><p><strong>Purpose: </strong>This study aimed to elucidate the mechanism by which JHT alleviates CSG, integrating network pharmacology, untargeted metabolomics, and gut microbiota analyses.</p><p><strong>Methods: </strong>The CSG rat model was established, and treatment effects were assessed via Hematoxylin and eosin (H&E) staining. The target profiles of JHT's components and the holistic targets of JHT were obtained. Enrichment analyses were performed on holistic targets and a multi-layer biomolecular network of JHT was established. The study also analyzed rat plasma for differential metabolites through untargeted metabolomics and evaluated the diversity and composition of gut microbiota in fecal and cecal contents samples using 16S rRNA sequencing.</p><p><strong>Results: </strong>JHT effectively reduced gastric inflammation in CSG rats. Network pharmacology indicated that diverse metabolic processes including lipid metabolism and nitric oxide metabolism play pivotal roles in the therapeutic effects of JHT on CSG. Metabolomics analysis identified differential metabolites, including betaine, which help enrich the gut microbiota. Phospholipids and citrulline indicate the severity of CSG. The pathway enrichment of differential metabolites confirmed the network pharmacology results and indicated the association with the gut microbiota. Through gut microbiota analyses, it was discovered that JHT could augment the gut microbiota by enhancing the abundance of betaine. Additionally, JHT was shown to boost the production of short-chain fatty acids (SCFAs) by increasing the abundances of Faecalibaculum and Bifidobacterium, consequently alleviating gastric inflammation in CSG.</p><p><strong>Conclusion: </strong>Our study revealed that JHT alleviated CSG through diverse metabolic processes including lipid and energy metabolism. Metabolites such as betaine, along with gut microbiota including Faecalibaculum and Bifidobacterium, play crucial roles in the therapeutic interventions. Our findings support the therapeutic potential of JHT and contribute to a deeper understanding of the role of TCM in the treatment of CSG.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"105"},"PeriodicalIF":5.3,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pien-Tze-Huang alleviates lithocholic acid-induced cholestasis in mice by shaping bile acid-submetabolome.","authors":"Yan Cao, Yanhong Zhai, Qihong Deng, Shufen Song, Wei Li, Youran Li, Yifan Lu, Jun Li, Zheng Cao, Yuelin Song","doi":"10.1186/s13020-025-01161-7","DOIUrl":"10.1186/s13020-025-01161-7","url":null,"abstract":"<p><strong>Background: </strong>Cholestasis is one of the most common and devastating manifestations of liver diseases. Although bile acid (BA) metabolism disturbances have been disclosed to be related to the etiopathogenesis of cholestasis, further research is desired to obtain an in-depth understanding of cholestasis. Additionally, only a limited number of treatment approaches are available for this disorder. Pien-Tze-Huang (PTH), a traditional Chinese medicine prescription, has been extensively utilized to treat various liver diseases. However, the effects of PTH on BA-submetabolome and the underlying mechanisms haven't been revealed.</p><p><strong>Methods: </strong>A strategy integrating widely targeted metabolomics, untargeted proteomics, and 16S rDNA sequencing, was employed to explore the regulatory effect and the mechanisms of PTH on BA-submetabolome of lithocholic acid (LCA)-induced cholestasis mice. Furthermore, LCA-induced injury HepG2 cells were deployed for efficacy justification and the mechanism exploration.</p><p><strong>Results: </strong>Both in vivo and in vitro assays demonstrated that PTH could protect liver against LCA-induced injury. Based on the quantitative BA-submetabolome migration and cell viability assays, 3-dehydroCA, CDCA, CA-7-S, HDCA, 3-ketocholanic acid, 7-ketoLCA, and 7,12-diketoLCA were identified as the key BA species correlating with hepatoprotective effects of PTH. Moreover, PTH restored the dramatically deflected BA-submetabolome in cholestasis mice through two different ways. On the one hand, the significantly decreased BA species can be directly supplemented during PTH administration or repaired via upregulating BA-related enzymes. On the other hand, the significantly increased BAs, such as T-β-MCA, TCDCA, TCA, TLCA, TMDCA, TUDCA, and TDCA, should be eliminated by the increased abundance of Lactobacillaceae and Lactobacillus.</p><p><strong>Conclusions: </strong>PTH alleviates cholestasis by synergistically regulating certain BA species, enzymes and gut microbiota, leading to holistic BA-submetabolome shaping.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"103"},"PeriodicalIF":5.3,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12225082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}