Department of Pharmacy, Tongling People's Hospital, Tongling, Anhui Province, China.
Department of Pharmacy, Tongling Sixth People's Hospital, Tongling, Anhui Province, China.
Medicine (Baltimore). 2024 Sep 13;103(37):e39725. doi: 10.1097/MD.0000000000039725.
Based on network pharmacology and molecular docking methods, to explore the possible targets and mechanisms of Bidens pilosa L. in treatment of liver fibrosis. The TCMSP, GeneCard, OMIM, TTD and DrugBank databases were used to obtain the targets of Bidens pilosa L and liver fibrosis, than the intersection targets were screened out by Venny 2.1.0, the protein-protein interaction (PPI) network and the core targets were obtained by the STRING database. Use Cytoscape3.7.2 software to draw the "traditional Chinese medicine-component-target-disease" network. The DAVID database platform was explored to analyze the biological process and pathway, and predict the anti-liver fibrosis mechanism of Bidens pilosa L. AutoDock and PyMol were used to verify the molecular docking between the active ingredients of Bidens pilosa L. and the core targets. Six active components of Bidens pilosa L. and 106 intersection targets were screened. PIK3R1, HSP90AA1, SRC, TP53, AKT1, RELA and other core targets were screened by PPI network analysis. The results of GO and KEGG enrichment analysis showed that the anti-liver fibrosis of Bidens pilosa L mainly involved in the regulation and negative regulation of apoptosis process, positive regulation of protein kinase B signal transduction, positive regulation of cell migration and other biological processes. Pathways acting on cancer, fluid shear stress and atherosclerosis, lipids and atherosclerosis, PI3K-AKT signaling pathway, MAPK signaling pathway and other signaling pathways. Molecular docking showed that the active components of Bidens pilosa L. displayed good binding activity with core target proteins, and the average binding energy was -7.47 kcal/mol. The possible mechanism of the active components against liver fibrosis is to regulate the PI3K-AKT, MAPK, and other signaling pathways by acting on core targets such as PIK3R1, HSP90AA1, SRC, TP53, AKT1, RELA, and induce the apoptosis of activated HSC cells to reverse and improve liver fibrosis.
基于网络药理学和分子对接方法，探讨三叶鬼针草治疗肝纤维化的可能靶点和作用机制。运用 TCMSP、GeneCard、OMIM、TTD 和 DrugBank 数据库获取三叶鬼针草和肝纤维化的作用靶点，应用 Venny 2.1.0 软件筛选交集靶点，利用 STRING 数据库构建蛋白互作（PPI）网络，获取核心靶点，采用 Cytoscape3.7.2 软件绘制“中药-成分-靶标-疾病”网络图。运用 DAVID 数据库平台对靶标进行生物过程和通路富集分析，预测三叶鬼针草抗肝纤维化的作用机制。采用 AutoDock 和 PyMol 软件对三叶鬼针草活性成分与核心靶标进行分子对接验证。筛选得到三叶鬼针草的 6 个活性成分和 106 个交集靶标，通过 PPI 网络分析筛选出 PIK3R1、HSP90AA1、SRC、TP53、AKT1、RELA 等核心靶标。GO 和 KEGG 富集分析结果表明，三叶鬼针草抗肝纤维化作用主要涉及凋亡过程的调控和负调控、蛋白激酶 B 信号转导的正调控、细胞迁移的正调控等生物过程，作用通路有癌症相关通路、流体剪切应激与动脉粥样硬化、脂类与动脉粥样硬化、PI3K-AKT 信号通路、MAPK 信号通路等。分子对接结果显示，三叶鬼针草活性成分与核心靶标蛋白结合活性较好，平均结合能为-7.47 kcal/mol。其活性成分可能通过作用于 PIK3R1、HSP90AA1、SRC、TP53、AKT1、RELA 等核心靶标，调控 PI3K-AKT、MAPK 等信号通路，诱导活化的 HSC 细胞凋亡，从而逆转和改善肝纤维化。
