基于网络药理学和分子对接探讨桂枝茯苓丸治疗慢性前列腺炎的作用机制

Mechanism of action of Guizhi Fuling Pill in treating chronic prostatitis based on network pharmacology and molecular docking

  • 摘要:
    目的 通过网络药理学和分子对接技术, 探讨桂枝茯苓丸治疗慢性前列腺炎的作用机制。
    方法 通过中药系统药理学数据库和分析平台(TCMSP)收集桂枝茯苓丸成分,从Swisstarget数据库获取靶点信息; 从GeneCards、OMIM、CTD及DisGeNET疾病库中筛查慢性前列腺炎靶点; 建立并分析蛋白质-蛋白质相互作用(PPI)网络; 采用DAVID数据库进行基因本体论(GO)功能注释与京都基因和基因组百科全书(KEGG)通路富集分析; 运用Cytoscape软件建立桂枝茯苓丸成分、靶点与慢性前列腺炎靶点的关联网络; 利用AutoDock Vina软件进行分子对接验证桂枝茯苓丸成分与靶点结合稳定性。
    结果 经TCMSP数据平台筛选去重后获得76个桂枝茯苓丸成分,Swisstarget数据库检索得到655个成分靶点; 桂枝茯苓丸与慢性前列腺炎交集靶点190个。GO分析结果显示,桂枝茯苓丸可能通过参与凋亡、ATP结合、信号转导等治疗慢性前列腺炎。KEGG分析提示,桂枝茯苓丸可调控磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B (AKT)、丝裂原活化蛋白激酶(MAPK)等通路干预慢性前列腺炎。分子对接数据显示,桂枝茯苓丸成分与靶点具有稳定构象。
    结论 桂枝茯苓丸成分可与靶点稳定结合,并通过多靶点、多途径发挥对慢性前列腺炎的治疗作用。

     

    Abstract:
    Objective To investigate the mechanism of action of Guizhi Fuling pill in treating chronic prostatitis (CP) using network pharmacology and molecular docking techniques.
    Methods Components of Guizhi Fuling pill were collected from the Traditional Chinese Medicines Systems Pharmacology Platform (TCMSP), and target information was obtained from the SwissTarget database. Targets for chronic prostatitis were screened from the GeneCards, OMIM, CTD, and DisGeNET disease databases. A protein-protein interaction (PPI) network was established and analyzed. Gene ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed using the DAVID database. The Cytoscape software was employed to construct an association network linking the components of Guizhi Fuling Pill, their targets, and the targets of chronic prostatitis. Molecular docking was conducted using AutoDock Vina software to verify the binding stability between the components of Guizhi Fuling pill and their targets.
    Results After screening and deduplication in the TCMSP database, 76 components of Guizhi Fuling Pill were identified, and 655 component targets were retrieved from the SwissTarget database. There were 190 intersecting targets between GuizhiFuling Pill and chronic prostatitis. GO analysis indicated that Guizhi Fuling Pill may treat chronic prostatitis by participating in processes such asapoptosis, ATP binding, and signal transduction. KEGG analysis suggested that Guizhi Fuling Pill can regulate pathways such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinase (MAPK) to intervene in chronic prostatitis. Molecular docking data demonstrated that the components of Guizhi Fuling pill exhibited stable conformations with their targets.
    Conclusion The components of Guizhi Fuling Pill can stably bind to their targets and exert therapeutic effects on chronic prostatitis through multiple targets and pathways.

     

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