Article(id=1291704828841972193, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704786705993936, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.20.014, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1757865600000, receivedDateStr=2025-09-15, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896029910, onlineDateStr=2026-08-05, pubDate=1761580800000, pubDateStr=2025-10-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896029910, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896029910, creator=13701087609, updateTime=1785896029910, updator=13701087609, issue=Issue{id=1291704786705993936, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='20', pageStart='2851', pageEnd='3000', issueExtLink='null', onlineDate='null', pubDate='1761580800000', pubDateStr='2025-10-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896019864, creator='13701087609', updateTime=1785896741492, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707813508702571, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704786705993936, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707813508702572, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704786705993936, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2929, endPage=2933, ext={EN=ArticleExt(id=1291704829064270306, articleId=1291704828841972193, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Screening of antioxidant targets for the treatment of Alzheimer’s disease based on network pharmacology, columnId=1246531412438966969, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Reader’s Field, runingTitle=null, highlight=null, articleAbstract=
Objective To systematically screen potential antioxidant targets for the treatment of Alzheimer’s disease (AD) based on network pharmacology strategy.
Methods Firstly, the structure-data file (SDF) of the antioxidant compound library was converted into the standard simplified molecular input line entry system (SMILES) molecular structure format usingrational discovery kit (RDKit), and then the potential targets of antioxidant compounds were predicted using the SwissTargetPrediction platform. After the obtained targets were analyzed with the differentially expressed genes of AD, a protein interaction network (PPI network) was constructed, and the functional interaction relationship was mined based on the STRING database. Further, the "compound-disease target-signaling pathway" network diagram was established with the help of Cytoscape software to screen key therapeutic targets. Finally, the core targets were annotated with Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis using the DAVID database.
Results Finally, 10 core targets with potential anti-Alzheimer’s disease effects were screened. Among them, the top three key nodes in degree value were heat shock protein 90α family class B member 1 (HSP90AB1), catenin β1 (CTNNB1) and proto-oncogene tyrosine protein kinase (SRC). Enrichment analysis suggested that these core targets may be mainly involved in the pathogenesis and intervention of Alzheimer’s disease through calcium signaling pathway and phosphatidyqinositol-3 kinase/protein kinase B (PI3K-Akt) signaling pathway, and had important therapeutic potential.
Conclusion This study systematically identified the core antioxidant targets and key pathways for the treatment of Alzheimer’s disease from the perspective of network pharmacology, providing theoretical support for further research on antioxidant drugs.
, authors=Jia-jia WANG
1, 2, Long-tu LI
2, Yu-meng ZHANG
1, 2, Zhi-yan LIU
2, Qian XIANG
1, 2, authorsList=Jia-jia WANG, Long-tu LI, Yu-meng ZHANG, Zhi-yan LIU, Qian XIANG, authorCompany=null, correspAuthors=Zhi-yan LIU, Qian XIANG, 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=1291704829517255139, articleId=1291704828841972193, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于网络药理学筛选治疗阿尔茨海默病的抗氧化靶点, columnId=1246531414020219657, journalTitle=中国临床药理学杂志, columnName=读者园地, runingTitle=null, highlight=null, articleAbstract=
目的 基于网络药理学策略，系统筛选潜在可用于治疗阿尔茨海默病（AD）的抗氧化靶点。
方法 首先利用化学信息学工具包（RDKit）将抗氧化化合物库的结构数据文件（SDF）转化为标准的SMILES分子结构格式，随后通过SwissTargetPrediction平台预测抗氧化化合物的潜在作用靶点。将所获得的靶点与AD差异表达基因进行交集分析后，构建蛋白质互作网络（PPI network），并基于STRING数据库进行功能互作关系挖掘。进一步借助Cytoscape软件建立“化合物–疾病靶点–信号通路”网络图，筛选关键治疗靶点。最后，使用DAVID数据库对核心靶点进行基因本体（GO）及京都基因与基因组百科全书（KEGG）功能富集分析。
结果 最终筛选得到10个具有潜在抗阿尔茨海默病作用的核心靶点。其中，Degree值排名前三的关键节点分别为：热休克蛋白90α家族B类成员1（HSP90AB1）、连环蛋白β1（CTNNB1）及原癌基因酪氨酸蛋白激酶（SRC）。富集分析提示，这些核心靶点可能主要通过钙信号通路（Calcium signaling pathway）和磷脂酰肌醇3激酶/蛋白激酶B（PI3K-Akt）信号通路等参与阿尔茨海默病的发病与干预过程，具有重要的治疗潜力。
结论 本研究从网络药理学角度系统识别了潜在的治疗阿尔茨海默病的核心抗氧化靶点与关键通路，为后续进一步研究抗氧化药物提供理论支持。
, authors=王佳佳
1, 2, 李龙图
2, 张雨萌
1, 2, 刘志艳
2, 向倩
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王佳佳（1999-），女，硕士研究生，主要从事临床药学方面的研究
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