基于网络药理学和分子对接的龙芪血脉合剂治疗动脉粥样硬化机制

Mechanism of Longqi Xuemai Heji in Treating Atherosclerosis Based on Network Pharmacology and Molecular Docking

摘要: 本研究旨在揭示龙芪血合剂(LQXMHJ)介入动脉粥样硬化(AS)的分子机制，采用网络药理与分子对接技术。通过整合TCMSP、HERB数据库，结合Uniport数据库对药物活性成分及其靶标进行筛选和基因标准化处理；AS相关靶点同时从GeneCards、OMIM和TTD数据库获取，通过交叉分析构建蛋白互作网络。GO功能注释和KEGG通路富集分析采用了David数据库，而分子对接验证则使用了AutodockTools软件。研究结果显示，LQXMHJ中126种活性成分(包括栎精、木犀等)可调控329个潜在靶点，其中涉及GAPDH、AKT1、IL6等关键靶点。通路分析揭示了其作用机理与通路密切相关，如AGE-RAGE信号转导，脂质代谢障碍，血流动力学改变等。分子对接校验显示，有效成分与目标蛋白的结合效果非常好。这些发现表明，LQXMHJ可能通过调节炎症反应、改善微循环和血液流变学特性的多成分–多靶点–多路径协同作用，发挥抗AS作用。该研究为后续深入探索LQXMHJ的药效物质基础和作用机理提供了重要的理论依据。

Abstract: This paper studies the molecular mechanism of Longqi Xuemai Heji (LQXMHJ), a classic Chinese herbal formula, in treating atherosclerosis (AS) using network pharmacology and molecular docking approaches. Active components and their targets were identified using the TCMSP and HERB databases, and gene standardization was subsequently performed through the UniProt database. Using the gene Cards, OMIM, and TTD databases as the source, an intersection analysis was used to construct a protein-protein interaction network for the AS-related targets. (GO) Ontology (GO) functional annotation and KEGG pathway enrichment analysis were done using the DAVID database and molecular docking validation was done using AutodockTools software. The data show that 126 active components in LQXMHJ (including quercetin, luteolin, etc.) regulate 329 possible targets, with important targets involving GAPDH, AKT1, IL6, and others. Pathway analysis linked its mechanism to AGE-RAGE signaling, lipid metabolism problems, and hemodynamic changes. A significant amount of binding affinities was found between the target proteins and the active components in molecular docking. These data show that LQXMHJ may exert anti-AS effects through multi-component, multi-target, multi-pathway synergistic effects, modulating inflammatory responses and improving microcirculation and blood flow properties. This work lays a theoretical basis for further research into LQXMHJ’s pharmacodynamic basis and mechanism of action.