Article(id=1291707061474185610, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.21.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1752508800000, receivedDateStr=2025-07-15, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896562212, onlineDateStr=2026-08-05, pubDate=1763308800000, pubDateStr=2025-11-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896562212, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896562212, creator=13701087609, updateTime=1785896562212, updator=13701087609, issue=Issue{id=1291706987964822180, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='21', pageStart='3001', pageEnd='3150', issueExtLink='null', onlineDate='null', pubDate='1763308800000', pubDateStr='2025-11-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896544684, creator='13701087609', updateTime=1785896721343, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707729324826977, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707729324826978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3049, endPage=3053, ext={EN=ArticleExt(id=1291707062141079947, articleId=1291707061474185610, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Recearch of unraveling the anti-inflammatory mechanism of Yinpu Jiedu tablet against diabetic kidney inflammation throgh network pharmacology and podocyte verification, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the main active components, potential targets and mechanisms of Yinpu Jiedu tablets in the treatment of diabetic renal inflammation by using network pharmacological methods and molecular docking techniques.
Methods The active ingredients of Yinpu jiede tables and therapeutic targets for diabetic kidney inflammation were retrieved from databases including TCMSP, PubChem, SwissTargetPrediction and GeneCards. A protein-protein interaction (PPI) network was constructed using Venny, STRING, Metascape, Bioinformatics and Cytoscape, followed by gene enrichment analysis. Molecular docking was performed using AutoDock, and the results were visualized with PyMOL. Furthermore, a lipopolysaccharide (LPS)-induced cellular model of diabetic kidney inflammation was established. The experiment included control group, model group (4 μmol·L-1 LPS) and experimantol group (30 μg·mL-1 Yinpu jiede tables). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to measure the messenger ribonucleic acid (mRNA) relative expression levels of AKT1 serine/threonine kinase 1(Akt1), tumor protein p53(Tp53), tumor necrosis factor-α (Tnf-α) and interleukin-6 (IL-6) to validate the network pharmacology predictions.
Results A total of 30 active ingredients and 435 potential targets of Yinpu jiede tables were identified. The core active ingredients included quercetin, luteolin, acacetin, morin and pelargonin. Intersection analysis between disease-related targets and drug-targets yielded 71 key genes, from which 4 core targets, inducling AKT1, TNF-α, IL-6 and TP53. Molecular docking results indicated strong binding affinity between the core active ingredients and the core targets. gene ontolog (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analyses suggested that Yinpu jiede tables exerts its therapeutic effects on diabetic kidney inflammation primarily through pathways such as pathways in cancer, the JAK-STAT signaling pathway, the AMPK signaling pathway and the Wnt signaling pathway. Cellular experiments confirmed that LPS induction significantly upregulated the mRNA expression of Akt1, Tp53, TNF-α, and IL-6 in podocytes, while treatment with Yinpu jiede tables effectively reversed this trend, restoring their expression to near-normal levels, thereby validating its regulatory role on the predicted targets and inflammatory pathways.
Conclusion Yinpu jiede tables may act on signal pathways such as JAK-STAT, AMPK, and Wnt through core targets such as AKT1, TNF, IL-6, and TP53, and exert therapeutic effects on diabetic kidney inflammation.
, authors=Jin-yuan ZHANG
1, 2, Li LAI
1, 2, Zi-yang LIN
3, 4, Ting-ting DUAN
3, 4, Jun-zheng YANG
3, 4, Yi-qi YANG
1, 2, authorsList=Jin-yuan ZHANG, Li LAI, Zi-yang LIN, Ting-ting DUAN, Jun-zheng YANG, Yi-qi YANG, authorCompany=null, correspAuthors=Yi-qi YANG, 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=1291707064234037644, articleId=1291707061474185610, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于网络药理学与足细胞验证探索银蒲解毒片治疗糖尿病肾炎的抗炎机制的研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 用网络药理学方法与分子对接技术,探讨银蒲解毒片治疗糖尿病肾炎的主要活性成分、作用靶点和信号通路。
方法 通过TCMSP、PubChem、SwissTargetPrediction及GeneCards等数据库获取银蒲解毒片的活性成分与疾病靶点;用Venny、STRING、Metascape、微生信及Cytoscape等工具构建蛋白质-蛋白质相互作用(PPI)网络,进行基因富集分析;运用AutoDock完成分子对接,PyMOL实现可视化验证。进一步建立脂多糖(LPS)诱导的糖尿病肾炎足细胞模型,设置对照组、模型组(4 μmol·L-1 LPS)与给药组(30 μg·mL-1银蒲解毒片),用反转录定量聚合酶链反应(RT-qPCR)检测AKT丝氨酸/苏氨酸激酶1(Akt1)、肿瘤蛋白p53(Tp53)、肿瘤坏死因子-α(TNF-α)及白细胞介素-6(IL-6)的信使RNA(mRNA)相对表达水平,以验证网络药理学预测结果。
结果 共筛选出30种活性成分和435个潜在靶点,核心活性成分为槲皮素、木犀草素、刺槐素、桑黄素和花葵苷。糖尿病肾炎疾病靶点集和药物治疗疾病靶点集进行交集分析后共得到71个关键基因,筛选出4个核心靶点即AKT1、TNF、IL-6和TP53。分子对接结果显示,核心活性成分与核心靶点具有良好的结合活性。基因本体论(GO)和京都基因与基因组百科全书(KEGG)富集分析提示,银蒲解毒片主要通过癌症通路、JAK-STAT信号途径、AMPK信号通路、Wnt信号通路等发挥治疗糖尿病肾炎的作用。细胞实验表明,LPS诱导后足细胞中Akt1、Tp53、TNF-α和IL-6 mRNA相对表达水平均显著上升,而银蒲解毒片干预可有效逆转该趋势,使其表达恢复至接近正常水平,证实其对预测靶点及炎症通路具有一定调控作用。
结论 银蒲解毒片可能通过AKT1、TNF、IL-6、TP53等核心靶点,作用于JAK-STAT、AMPK、Wnt等信号通路,发挥对糖尿病肾炎治疗作用。
, authors=张津源
1, 2, 赖丽
1, 2, 林子扬
3, 4, 段婷婷
3, 4, 杨军政
3, 4, 杨祎琦
1, 2, authorsList=张津源, 赖丽, 林子扬, 段婷婷, 杨军政, 杨祎琦, authorCompany=null, correspAuthors=杨祎琦, authorNote=
张津源(2000-),男,硕士研究生,主要从事中西医结合防治糖尿病肾病的相关研究
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1.Guangdong Pharmaceutical University, Guangzhou, Guangdong 510000, China
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1.广东药科大学,广东 广州 510000
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张津源(2000-),男,硕士研究生,主要从事中西医结合防治糖尿病肾病的相关研究
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1.Guangdong Pharmaceutical University, Guangzhou, Guangdong 510000, China
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3.Guangzhou Consun Pharmaceutical Co., Ltd., Guangzhou, Guangdong 510765, China
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3.广州康臣药业有限公司,广东 广州 510765
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3.Guangzhou Consun Pharmaceutical Co., Ltd., Guangzhou, Guangdong 510765, China
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3.广州康臣药业有限公司,广东 广州 510765
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