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Article(id=1292126585629471587, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126460546929080, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.03.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1765814400000, receivedDateStr=2025-12-16, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996584565, onlineDateStr=2026-08-06, pubDate=1771257600000, pubDateStr=2026-02-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996584565, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996584565, creator=13701087609, updateTime=1785996584565, updator=13701087609, issue=Issue{id=1292126460546929080, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='3', pageStart='301', pageEnd='450', issueExtLink='null', onlineDate='null', pubDate='1771257600000', pubDateStr='2026-02-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996554742, creator='13701087609', updateTime=1786014541627, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201903060963536, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126460546929080, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201903060963537, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126460546929080, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=393, endPage=398, ext={EN=ArticleExt(id=1292126585847575396, articleId=1292126585629471587, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Exploring the mechanism of Qizhi hypoglycemic tablets in treating diabetic vascular complications based on network pharmacology and molecular docking, columnId=1246531412438966969, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Reader’s Field, runingTitle=null, highlight=null, articleAbstract=
Objective

To systematically elucidate the mechanism of action of Qizhi hypoglycemic tablets (QZT) in treating diabetic vascular complications, this study adopted the methods of network pharmacology and molecular docking.

Methods

Active ingredients and their corresponding targets of QZT were retrieved from traditional Chinese medicine systems pharmacology database and analysis platform (TCMSP) and other databases. Disease targets related to diabetic nephropathy, retinopathy, and peripheral neuropathy were collected from The human gene database (GeneCards) and online mendelian inheritance in man (OMIM). Overlapping targets between drugs and diseases were identified, and a protein-protein interaction (PPI) network was constructed. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) enrichment analyses were performed using the database for annotation, visualization, and integrated discovery (DAVID). Molecular docking was used to validate the binding interactions between key active components and core targets.

Results

A total of 116 active ingredients, 2 245 disease-related targets, and 354 common targets were obtained. Core targets such as proto-oncogene tyrosine-protein kinase (SRC), signal transducer and activator of transcription 3 (STAT3), estrogen receptor 1 (ESR1), and RAC-alpha serine/threonine-protein kinase (AKT1) were identified. GO and KEGG analyses revealed that the therapeutic effects of QZT were primarily mediated through key pathways including phosphatidylinositol 3-kinase/Akt signaling pathway (PI3K-Akt) and advanced glycation end products-receptor for advanced glycation end products signaling pathway (AGE-RAGE). Molecular docking confirmed stable binding of core components including apigenin, baicalein, and 4′,7-dihydroxyflavanone (DFV) to the core targets.

Conclusion

This study preliminarily clarifies the multi-component, multi-target, and multi-pathway mechanism of QZT against diabetic vascular complications, providing a theoretical basis for its clinical application and further investigation.

, authors=Yao-qi WEN1, Zhen-lin WANG1, Yu-qing CHEN1, Xiu-qing ZHU1, Miao-ling TU1, 2, Yu-guan WEN1, 2, authorsList=Yao-qi WEN, Zhen-lin WANG, Yu-qing CHEN, Xiu-qing ZHU, Miao-ling TU, Yu-guan WEN, authorCompany=null, correspAuthors=Yu-guan WEN, 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=1292126586095039333, articleId=1292126585629471587, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于网络药理学和分子对接探讨芪蛭降糖片治疗糖尿病血管并发症的作用机制, columnId=1246531414020219657, journalTitle=中国临床药理学杂志, columnName=读者园地, runingTitle=null, highlight=null, articleAbstract=
目的

本研究旨在通过网络药理学和分子对接系统性揭示芪蛭降糖片（QZT）治疗糖尿病血管并发症的作用机制。

方法

用中药系统药理学数据库与分析平台（TCMSP）等数据库筛选复方活性成分及其靶点。人类基因数据库（GeneCards）和在线人类孟德尔遗传数据库（OMIM）等数据库获取糖尿病肾病、视网膜病变和周围神经病变疾病靶点，获取共有靶点，构建蛋白质互作网络。利用注释、可视化与整合发现数据库（DAVID）数据库进行基因本体（GO）和京都基因与基因组百科全书（KEGG）富集分析，并最终采用分子对接验证关键成分与核心靶点间的相互作用。

结果

共获得116种活性成分、2 245个疾病靶点及354个共有靶点；核心靶点包括原癌基因酪氨酸蛋白激酶（SRC）、信号转导和转录激活因子3（STAT3）、雌激素受体1（ESR1）、RAC-α丝氨酸/苏氨酸蛋白激酶（AKT1）等。GO和KEGG富集分析提示，复方成分主要经由磷脂酰肌醇3-激酶-蛋白激酶B信号通路（PI3K-Akt）、晚期糖基化终产物-晚期糖基化终产物受体信号通路（AGE-RAGE）等通路发挥作用。分子对接结果证实，芹菜素、黄芩素、4′，7-二羟基黄烷酮（DFV）等核心成分与核心靶点结合稳定。

结论

本研究初步阐明了芪蛭降糖片通过多成分、多靶点、多通路协同作用于糖尿病血管并发症的治疗机制，为该复方的临床应用和后续研究提供了理论基础。

, authors=温耀祺1, 王震霖1, 陈玉清1, 朱秀清1, 涂妙龄1, 2, 温预关1, 2, authorsList=温耀祺, 王震霖, 陈玉清, 朱秀清, 涂妙龄, 温预关, authorCompany=null, correspAuthors=温预关, authorNote=

温耀祺（2002-），男，硕士研究生，主要从事临床药学与药物评价方面的研究

, correspAuthorsNote=
温预关，主任药师，硕士生导师 Tel: （020）81268389 E-mail:
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温耀祺（2002-），男，硕士研究生，主要从事临床药学与药物评价方面的研究

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温耀祺（2002-），男，硕士研究生，主要从事临床药学与药物评价方面的研究

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基于网络药理学和分子对接探讨芪蛭降糖片治疗糖尿病血管并发症的作用机制
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温耀祺 1 , 王震霖 1 , 陈玉清 1 , 朱秀清 1 , 涂妙龄 1, 2 , 温预关 1, 2
中国临床药理学杂志 | 读者园地 2026,42(3): 393-398
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中国临床药理学杂志 |读者园地 2026 , 42 (3) : 393 -398
基于网络药理学和分子对接探讨芪蛭降糖片治疗糖尿病血管并发症的作用机制
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温耀祺1, 王震霖1, 陈玉清1, 朱秀清1, 涂妙龄1, 2, 温预关1, 2
作者信息
  • 1.广州医科大学 附属脑科医院Ⅰ期临床研究室，广东 广州 510370
  • 2.广东省精神疾病转化医学工程技术研究中心，广东 广州 510370
通讯作者:
温预关，主任药师，硕士生导师 Tel: （020）81268389 E-mail:
作者简介:

温耀祺（2002-），男，硕士研究生，主要从事临床药学与药物评价方面的研究

Exploring the mechanism of Qizhi hypoglycemic tablets in treating diabetic vascular complications based on network pharmacology and molecular docking
Yao-qi WEN1, Zhen-lin WANG1, Yu-qing CHEN1, Xiu-qing ZHU1, Miao-ling TU1, 2, Yu-guan WEN1, 2
Affiliations
  • 1.Phase Ⅰ Clinical Research Laboratory, The Affiliated Brain Hospital of Guangzhou Medical University, Guangzhou 510370, Guangdong Province, China
  • 2.Guangdong Engineering Technology Research Center for Translational Medicine of Mental Disorders, Guangzhou 510370, Guangdong Province, China
出版时间: 2026-02-17 doi: 10.13699/j.cnki.1001-6821.2026.03.015
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目的

本研究旨在通过网络药理学和分子对接系统性揭示芪蛭降糖片（QZT）治疗糖尿病血管并发症的作用机制。

方法

用中药系统药理学数据库与分析平台（TCMSP）等数据库筛选复方活性成分及其靶点。人类基因数据库（GeneCards）和在线人类孟德尔遗传数据库（OMIM）等数据库获取糖尿病肾病、视网膜病变和周围神经病变疾病靶点，获取共有靶点，构建蛋白质互作网络。利用注释、可视化与整合发现数据库（DAVID）数据库进行基因本体（GO）和京都基因与基因组百科全书（KEGG）富集分析，并最终采用分子对接验证关键成分与核心靶点间的相互作用。

结果

共获得116种活性成分、2 245个疾病靶点及354个共有靶点；核心靶点包括原癌基因酪氨酸蛋白激酶（SRC）、信号转导和转录激活因子3（STAT3）、雌激素受体1（ESR1）、RAC-α丝氨酸/苏氨酸蛋白激酶（AKT1）等。GO和KEGG富集分析提示，复方成分主要经由磷脂酰肌醇3-激酶-蛋白激酶B信号通路（PI3K-Akt）、晚期糖基化终产物-晚期糖基化终产物受体信号通路（AGE-RAGE）等通路发挥作用。分子对接结果证实，芹菜素、黄芩素、4′，7-二羟基黄烷酮（DFV）等核心成分与核心靶点结合稳定。

结论

本研究初步阐明了芪蛭降糖片通过多成分、多靶点、多通路协同作用于糖尿病血管并发症的治疗机制，为该复方的临床应用和后续研究提供了理论基础。

芪蛭降糖片  /  糖尿病血管并发症  /  网络药理学  /  分子对接
Objective

To systematically elucidate the mechanism of action of Qizhi hypoglycemic tablets (QZT) in treating diabetic vascular complications, this study adopted the methods of network pharmacology and molecular docking.

Methods

Active ingredients and their corresponding targets of QZT were retrieved from traditional Chinese medicine systems pharmacology database and analysis platform (TCMSP) and other databases. Disease targets related to diabetic nephropathy, retinopathy, and peripheral neuropathy were collected from The human gene database (GeneCards) and online mendelian inheritance in man (OMIM). Overlapping targets between drugs and diseases were identified, and a protein-protein interaction (PPI) network was constructed. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) enrichment analyses were performed using the database for annotation, visualization, and integrated discovery (DAVID). Molecular docking was used to validate the binding interactions between key active components and core targets.

Results

A total of 116 active ingredients, 2 245 disease-related targets, and 354 common targets were obtained. Core targets such as proto-oncogene tyrosine-protein kinase (SRC), signal transducer and activator of transcription 3 (STAT3), estrogen receptor 1 (ESR1), and RAC-alpha serine/threonine-protein kinase (AKT1) were identified. GO and KEGG analyses revealed that the therapeutic effects of QZT were primarily mediated through key pathways including phosphatidylinositol 3-kinase/Akt signaling pathway (PI3K-Akt) and advanced glycation end products-receptor for advanced glycation end products signaling pathway (AGE-RAGE). Molecular docking confirmed stable binding of core components including apigenin, baicalein, and 4′,7-dihydroxyflavanone (DFV) to the core targets.

Conclusion

This study preliminarily clarifies the multi-component, multi-target, and multi-pathway mechanism of QZT against diabetic vascular complications, providing a theoretical basis for its clinical application and further investigation.

Qizhi hypoglycemic tablets  /  diabetic vascular complications  /  network pharmacology  /  molecular docking
温耀祺, 王震霖, 陈玉清, 朱秀清, 涂妙龄, 温预关. 基于网络药理学和分子对接探讨芪蛭降糖片治疗糖尿病血管并发症的作用机制. 中国临床药理学杂志, 2026 , 42 (3) : 393 -398 . DOI: 10.13699/j.cnki.1001-6821.2026.03.015
Yao-qi WEN, Zhen-lin WANG, Yu-qing CHEN, Xiu-qing ZHU, Miao-ling TU, Yu-guan WEN. Exploring the mechanism of Qizhi hypoglycemic tablets in treating diabetic vascular complications based on network pharmacology and molecular docking[J]. Chinese Journal of Clinical Pharmacology, 2026 , 42 (3) : 393 -398 . DOI: 10.13699/j.cnki.1001-6821.2026.03.015
基金
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  • 中华国际医学交流基金资助项目(Z-2014-8-2309-5)
  • 广东省药学会扬子江基金资助项目(2025A01033)
  • 广东省医院药学研究基金（澳美基金）资助项目(2024A34)
  • 广东省医学科研基金资助项目(A2024493; A2024771; A2025225)
  • 广东省药学会罕见病超说明书用药评价研究科研基金项目(2025HJB01014)
  • 2025年广东省医院药学研究基金（康缘基金）项目(2025A03025)
  • 广州市临床重点专科（临床医学研究所）基金资助项目
  • 重大疑难疾病中西医临床协作项目(国中医药综结合发【2024】3号)
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doi: 10.13699/j.cnki.1001-6821.2026.03.015
  • 接收时间：2025-12-16
  • 首发时间：2026-08-06
  • 出版时间：2026-02-17
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  • 收稿日期：2025-12-16
基金
中华国际医学交流基金资助项目(Z-2014-8-2309-5)
广东省药学会扬子江基金资助项目(2025A01033)
广东省医院药学研究基金（澳美基金）资助项目(2024A34)
广东省医学科研基金资助项目(A2024493; A2024771; A2025225)
广东省药学会罕见病超说明书用药评价研究科研基金项目(2025HJB01014)
2025年广东省医院药学研究基金（康缘基金）项目(2025A03025)
广州市临床重点专科（临床医学研究所）基金资助项目
重大疑难疾病中西医临床协作项目(国中医药综结合发【2024】3号)
作者信息
    1.广州医科大学 附属脑科医院Ⅰ期临床研究室，广东 广州 510370
    2.广东省精神疾病转化医学工程技术研究中心，广东 广州 510370

通讯作者:

温预关，主任药师，硕士生导师 Tel: （020）81268389 E-mail:
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https://castjournals.cast.org.cn/joweb/zglcylxzz/CN/10.13699/j.cnki.1001-6821.2026.03.015
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Percentage of
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
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