Article(id=1276976152778507116, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250813.401, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1751990400000, receivedDateStr=2025-07-09, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384439892, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384439892, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384439892, creator=13701087609, updateTime=1782384439892, updator=13701087609, issue=Issue{id=1276976057215488893, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='2', pageStart='301', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1768406400000', pubDateStr='2026-01-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782384417107, creator='13701087609', updateTime=1782384524478, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976507658563977, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976507658563978, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=533, endPage=542, ext={EN=ArticleExt(id=1276976152996610926, articleId=1276976152778507116, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Amelioration of inflammatory response in mice with non-alcoholic fatty liver disease via Modified Wushi Xiexin Decoction by inhibiting TLR4/NF-κB pathway, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide, characterized primarily by hepatic inflammation and dysregulated lipid metabolism. As a classic representative formula of the "bitter-purging method", Modified Wushi Xiexin Decoction has demonstrated definite clinical efficacy; however, its anti-inflammatory effects and underlying mechanisms in the treatment of NAFLD remain unclear. This study combines network pharmacology with animal experimental validation to evaluate the therapeutic effect of Modified Wushi Xiexin Decoction on NAFLD and reveal its potential mechanisms of action. Drug targets were collected from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). NAFLD-related disease targets were retrieved from the Therapeutic Target Database (TTD), GeneCards, Online Mendelian Inheritance in Man (OMIM), Pharmacogenomics Knowledge Base (PharmGKB), and Comparative Toxicogenomics Database (CTD). R software was used to screen the intersection targets of the two sets. Core target analysis and network visualization were performed by using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database and Cytoscape 3.8.2 software. R software was applied for Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Core targets were analyzed based on the Gene Expression Omnibus (GEO) database, and receiver operating characteristic (ROC) curves were plotted to evaluate the diagnostic efficacy of the core targets. For animal experimental validation, a NAFLD mouse model was established by feeding a 60% high-fat diet combined with intraperitoneal injection of streptozotocin. Pathological improvements were assessed by hematoxylin-eosin (HE) staining and oil red O staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the level of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in liver tissue. Immunohistochemistry (IHC) and Western blot (WB) were performed to measure the expression of Toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB), and NOD-like receptor protein 3 (NLRP3) proteins in mouse liver tissue. Network pharmacology identified 97 active components, 108 intersection targets, and 10 core targets of Modified Wushi Xiexin Decoction. GO enrichment analysis indicated that anti-NAFLD effects were exerted by regulating biological processes such as oxidative stress and nutritional levels. KEGG enrichment analysis mainly involved signaling pathways, including TLR, NF-κB, and TNF. The GEO database indicates that there is a significant difference in TLR4 expression between healthy individuals and NAFLD patients (P<0.05), with the area under the ROC curve (AUC) being greater than 0.810, suggesting a high diagnostic efficacy. Animal experiments showed that Modified Wushi Xiexin Decoction could alleviate pathological damage in the liver tissue of NAFLD mice, reduce blood lipids, improve liver function, and downregulate the expression of inflammatory factors in liver tissue. IHC and WB confirmed that Modified Wushi Xiexin Decoction could downregulate the TLR4 expression, inhibit NF-κB activity, and suppress NLRP3 inflammasome activation. In conclusion, Modified Wushi Xiexin Decoction may alleviate inflammatory responses and improve liver function and blood lipids in NAFLD by regulating the TLR4/NF-κB signaling pathway and inhibiting NLRP3 inflammasome activation, thereby exerting therapeutic effects on NAFLD.

, authors=null, authorsList=Li-juan DAN, Yu-qiao LIU, Yan-wei HAO, Hong-fei SONG, Xiu-yan LI, Xiao-jie YOU, Dong WANG, Jie MU, Qiao LI, authorCompany=null, correspAuthors=Jie MU, Qiao LI, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1276976153227297648, articleId=1276976152778507116, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=吴氏泻心汤加减方通过抑制TLR4/NF-κB通路改善小鼠非酒精性脂肪性肝病的炎症反应, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

非酒精性脂肪性肝病（NAFLD）是全球最常见的慢性肝病，以肝脏炎症和脂质代谢紊乱为主要特征。吴氏泻心汤加减方作为苦泄法经典代表方剂，临床疗效确切，但其治疗NAFLD的抗炎作用及机制尚未明确。该研究结合网络药理学与动物实验验证，评价吴氏泻心汤加减方对NAFLD的治疗效果并揭示其潜在作用机制。通过中药系统药理学平台（TCMSP）数据库收集药物作用靶点，从TTD、GeneCards、OMIM、PharmGKB、CTD数据库获取NAFLD疾病靶点，利用R软件筛选二者交集靶点；通过STRING数据库及Cytoscape 3.8.2软件进行核心靶点分析与网络可视化，采用R软件进行基因本体论（GO）富集分析与京都基因与基因组百科全书（KEGG）通路富集分析；基于GEO数据库分析核心靶点，绘制受试者工作特征（ROC）曲线评估其诊断效能。动物实验验证采用60%高脂饲料联合腹腔注射链脲佐菌素构建NAFLD小鼠模型；HE染色及油红O染色评估病理改善；ELISA检测肝组织肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）含量；免疫组化及蛋白免疫印迹法检测小鼠肝组织Toll样受体4（TLR4）、核因子κB（NF-κB）、NOD样受体蛋白3（NLRP3）蛋白表达。网络药理学筛选出吴氏泻心汤加减方活性成分97个，交集靶点108个及核心靶点10个；GO富集分析显示其通过调节氧化应激、营养水平等生物学过程发挥抗NAFLD作用；KEGG富集分析主要涉及TLR、NF-κB、TNF等信号通路。GEO数据库提示TLR4在健康者与NAFLD患者中存在差异（P<0.05），ROC曲线下面积（AUC）>0.810，诊断效能较高。动物实验显示，吴氏泻心汤加减方可减轻NAFLD小鼠肝组织病理损伤，降低血脂，改善肝功能，下调肝组织炎症因子表达；免疫组化及蛋白免疫印迹法检测证实其可下调TLR4表达，抑制NF-κB活性及NLRP3炎性小体激活。综上，吴氏泻心汤加减方可能通过调控TLR4/NF-κB信号通路、抑制NLRP3炎性小体活化，进而减轻NAFLD炎症反应，改善肝功能及血脂，发挥NAFLD治疗作用。

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淡丽娟，博士研究生，E-mail: dljaniuan@163.com

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淡丽娟，博士研究生，E-mail: dljaniuan@163.com

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