基于网络药理学探讨京尼平苷治疗动脉粥样硬化的作用机制  

Exploring the Mechanism of Geniposide in Treating Atherosclerosis Based on Network Pharmacology

作　　者：胡雨蝶 杨阳 田维毅 Hu Yudie;Yang Yang;Tian Weiyi(School of Basic Medicine,Guizhou University of Traditional Chinese Medicine,Guiyang 550025,China)

机构地区：[1]贵州中医药大学基础医学院,贵州贵阳550025

出　　处：《巴楚医学》2024年第4期45-53,共9页Bachu Medical Journal

基　　金：国家自然科学基金项目(No:81760790)。

摘　　要：目的:本研究旨在通过网络药理学深入剖析京尼平苷(Gen)在抗动脉粥样硬化(AS)过程中的潜在作用机制。方法:检索TCMSP、SwissTargetPrediction等权威数据库,精准预测并筛选出Gen的活性靶点。同时,借助OMIM、GeneCards等数据库,全面收集AS疾病的相关靶点。随后,通过Venny在线工具,高效地找出AS与Gen之间的交集靶点。为了更直观地展示这些关系,使用Cytoscape 3.9.1软件绘制活性成分与靶点的网络图。进一步利用STRING数据库和Metascape数据库,深入分析蛋白-蛋白相互作用(PPI)以及靶点的富集情况。最后,通过SYBYL-X 2.0软件,对关键靶点进行模拟分子对接。结果:预测出Gen的活性靶点171个,AS的靶点则多达5 646个。在这两者之中,发现了118个交集基因。进一步的分析表明,Gen在治疗AS的过程中,主要通过调节丝裂原活化蛋白激酶(MAPK)信号通路,影响白细胞介素6(IL-6)、白细胞介素1β(IL-1β)和表皮生长因子受体(EGFR)等关键靶点。分子对接的结果也进一步证实,Gen与丝裂原活化蛋白激酶14(MAPK14)、JUN和PTEN等靶点具有优异的结合能力。结论:本研究表明,Gen可能通过MAPK信号通路,影响MAPK14、JUN和PTEN等基因,从而在AS的治疗中发挥重要作用。这一发现不仅为AS的治疗提供了新的思路,也为后续的实验研究奠定了坚实的基础。Objective:To investigate the mechanism of geniposide(Gen)in anti-atherosclerosis(AS)through network pharmacology.Methods:We searched authoritative databases such as TCMSP and SwissTargetPrediction to accurately predict and screen out the active targets of Gen.Meanwhile,we comprehensively collected relevant targets of AS with the help of databases such as OMIM and GeneCards.Subsequently,we efficiently identified the intersection targets between AS and Gen through the Venny online tool.To visually display these relationships,we used Cytoscape 3.9.1 software to draw a network diagram of active components and targets.Furthermore,we utilized the STRING and Metascape databases to deeply analyze protein-protein interactions(PPI)and target enrichment.Finally,we simulated molecular docking of key targets using SYBYL-X 2.0 software. Results: A total of 171 active targets for Gen and up to 5 646 targets for AS were predicted. Among them, we discovered 118 intersection genes. Further analysis revealed that Gen exerts its therapeutic effects on AS primarily by mediating the mitogen-activated protein kinase (MAPK) signaling pathway and influencing key targets such as interleukin-6 (IL-6), interleukin-1β (IL-1β), and epidermal growth factor receptor (EGFR). The results of molecular docking further confirmed that Gen has excellent binding capabilities with targets such as MAPK14, JUN, and PTEN. Conclusion: This study suggests that Gen may play a crucial role in the treatment of AS by affecting genes such as MAPK14, JUN, and PTEN through the MAPK signaling pathway. This discovery not only provides new insights into the treatment of AS but also lays a solid foundation for subsequent experimental research.

关 键 词：京尼平苷 动脉粥样硬化 分子对接 

分 类 号：R543[医药卫生—心血管疾病]