Article(id=1292765505195103052, tenantId=1146029695717560320, journalId=1291416979304972313, issueId=1291824268032110598, articleNumber=null, orderNo=null, doi=10.3969/j.issn.1005-4847.2026.03.004, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1749657600000, receivedDateStr=2025-06-12, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1786148914859, onlineDateStr=2026-08-08, pubDate=1774800000000, pubDateStr=2026-03-30, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1786148914859, onlineIssueDateStr=2026-08-08, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1786148914859, creator=13701087609, updateTime=1786148914859, updator=13701087609, issue=Issue{id=1291824268032110598, tenantId=1146029695717560320, journalId=1291416979304972313, year='2026', volume='34', issue='3', pageStart='313', pageEnd='468', issueExtLink='null', onlineDate='null', pubDate='1774800000000', pubDateStr='2026-03-30', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1785924506432, creator='ztmeta', updateTime=1786331936953, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1293533155567366441, tenantId=1146029695717560320, journalId=1291416979304972313, issueId=1291824268032110598, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1293533155567366442, tenantId=1146029695717560320, journalId=1291416979304972313, issueId=1291824268032110598, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=352, endPage=361, ext={EN=ArticleExt(id=1292765506935739213, articleId=1292765505195103052, tenantId=1146029695717560320, journalId=1291416979304972313, language=EN, title=Mechanism of Buzhong Yiqi Decoction in ameliorating chemotherapy-induced sarcopenia investigated by network pharmacology, molecular docking and experimental validation, columnId=null, journalTitle=Acta Laboratorium Animalis Scientia Sinica, columnName=null, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the potential active components and underlying mechanisms of Buzhong Yiqi Decoction (BZYQD) in ameliorating chemotherapy-induced sarcopenia (CIS) using integrated strategies of network pharmacology and in vivo validation.
Methods The active components of BZYQD and their targets were identified using the TCMSP platform. CIS-related targets were obtained from the GeneCards and OMIM databases. We constructed a protein-protein interaction network by taking the intersection targets of drugs and diseases and identifying the core targets. We carried out gene ontology (GO) functional annotation and kyoto encyclopedia of genes and genomes pathway (KEGG) enrichment. Molecular docking and visualization were performed using AutodockTools 1.5.7 and PyMOL 2.7.1. The therapeutic effects of BZYQD on CIS were validated in animal experiments.
Results The core targets at the drugs/diseases intersection included Akt1, TP53, tumor necrosis factor (TNF), interleukin (IL)-1β, and IL-6. Molecular docking analysis indicated that the core targets and main active components had favorable binding affinities. In the experiment on SD rats, body mass, grip strength, exhaustive swimming time, and myofiber cross-sectional area were significantly decreased in the model (M group) compared with the control group (C group). Serum levels of TNF-α, IL-1β, and IL-6 detected by enzyme-linked immunosorbent assay were significantly elevated. The phospho (p)-nuclear factor (NF)-κB p65/NF-κB p65 ratio was significantly increased, while the p-Akt/Akt and p-phosphoinositide 3-kinase (PI3K)/PI3K ratios were significantly decreased, as shown by Western Blot. Administration of BZYQD ameliorated these alterations in a dose-dependent manner, with the most pronounced effects in the HBYD group.
Conclusions BZYQD may improve CIS by regulating the PI3K/Akt/NF-κB signaling pathway.
, authors=Yueyu ZHANG
1, Yi WANG
1, Xiande MA
2, Siqi ZHANG
1, Ping LEI
1, *, authorsList=Yueyu ZHANG, Yi WANG, Xiande MA, Siqi ZHANG, Ping LEI, authorCompany=null, correspAuthors=Ping LEI, authorNote=null, correspAuthorsNote=
, 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=1292765507254506318, articleId=1292765505195103052, tenantId=1146029695717560320, journalId=1291416979304972313, language=CN, title=基于网络药理学、分子对接和动物实验探讨补中益气汤改善化疗肌少症的机制, columnId=1292765498584888180, journalTitle=中国实验动物学报, columnName=研究报告, runingTitle=null, highlight=null, articleAbstract=
目的 采用网络药理学与体内实验，探讨补中益气汤（Buzhong Yiqi Decoction, BZYQD）改善化疗肌少症（chemotherapy-induced sarcopenia, CIS）的潜在活性成分及作用机制。
方法 利用TCMSP筛选BZYQD活性成分及靶点；通过GeneCards和OMIM数据库筛选CIS疾病靶点。取药物与疾病交集靶点构建蛋白互作网络，识别核心靶点，进行GO功能注释及KEGG通路富集。利用AutodockTools 1.5.7和PyMOL 2.7.1进行分子对接及可视化处理。通过动物实验验证BZYQD改善CIS的效果。
结果 药物与疾病交集的核心靶点，包括Akt1、TP53、TNF、IL-1β、IL-6等。分子对接核心靶点与主要活性成分大部分具有较好结合能力。在SD大鼠实验中，相较于空白组（C组），模型组（M组）体质量、抓力和力竭游泳时间与肌丝横截面积显著降低，ELISA检测血清中TNF-α、IL-1β、IL-6的含量显著升高，Western Blot检测显示，骨骼肌p-NF-κB p65/NF-κB p65比值显著升高，p-Akt/Akt和p-PI3K/PI3K比值显著降低；BZYQD各剂量组大鼠上述指标均有所改善，其中高剂量组（HBYD组）效果最为显著。
结论 BZYQD可能通过调节PI3K/Akt/NF-κB信号通路改善CIS。
, authors=张月宇
1, 王艺
1, 马贤德
2, 张思琦
1, 雷萍
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