基于网络药理学分析茵陈–荷叶治疗非酒精性脂肪性肝病的作用机制

Analysis the Mechanism of Herba Artemisiae scopariae and Folium nelumbinis in the Treatment of Non-Alcoholic Fatty Liver Disease Based on Network Pharmacology

摘要: 目的：通过网络药理学筛选茵陈–荷叶治疗非酒精性脂肪性肝病的有效成分和靶点。方法：应用TCMSP和SWISS数据库查找茵陈、荷叶的活性成分及其靶点，通过OMIM和GeneCards数据库检索非酒精性脂肪性肝病的相关靶点，并获取交集靶点。利用Cytoscape 3.10.3构建茵陈–荷叶与非酒精性脂肪性肝病之间的“药物–成分–疾病–靶点”网络图，筛选出关键靶点，并进行GO和KEGG富集分析。结果：得到茵陈–荷叶的有效活性成分共24个，交集靶点为183个。通过蛋白互作分析(PPI)，识别出核心靶点包括TP53、AKT1、JUN、HSP90AA1、STAT3、TNF、IL6、MAPK1、HSP90AB1、BCL2等。KEGG和GO分析结果显示，主要影响的生物过程包括耐受性诱导、T细胞耐受性诱导的调节以及肽类激素处理等10种类型；涉及的细胞成分包括轴丝动力蛋白复合体、质膜和细胞质区域等10种类型；主要的分子功能包括细胞因子活性、相同蛋白质结合等10种功能。研究表明，这些成分主要通过脂质代谢与动脉粥样硬化、内分泌抵抗等通路对非酒精性脂肪性肝病发挥作用。结论：茵陈–荷叶改善非酒精性脂肪性肝病的作用机制可能通过内分泌抵抗、脂质与动脉粥样硬化等多条通路实现，其特点在于具有多个靶点和多个成分。

Abstract: Objective: The effective ingredients and targets of Artemisiae scopariae and Folium nelumbinis leaves to treat non-alcoholic fatty liver disease through network pharmacology. Methods: The TCMSP and SWISS databases were utilized to identify the active ingredients and targets of Artemisiae scopariae and Folium nelumbinis. Additionally, the OMIM and Genecards databases were searched to explore non-alcoholic fatty liver disease and to obtain intersection targets. Cytoscape 3.10.3 was employed to construct a “drug-ingredient-disease-target” network diagram linking Artemisiae scopariae and Folium nelumbinis to non-alcoholic fatty liver disease. Key targets were screened, and GO and KEGG enrichment analyses were conducted. Results: There are 24 effective active ingredients derived from Artemisiae scopariae and Folium nelumbinis, which interact with 183 common targets. The analysis of protein-protein interactions (PPI) identifies core targets such as TP53, AKT1, JUN, HSP90AA1, STAT3, TNF, IL6, MAPK1, HSP90AB1, and BCL2. Results from KEGG and GO analyses indicate that the primary biological processes influenced include 10 types of tolerance induction, T-cell tolerance induction, and peptide hormone processing. Additionally, 10 cellular components have been identified, including the axonemal dynein complex, axoneme, and ciliary plasm. The analysis also highlights 10 molecular functions, such as ATP-dependent microtubule motor activity, minus-end-directed dynein light intermediate chain binding, and dynein intermediate chain binding. Studies suggest that these components primarily exert their effects through pathways related to lipid metabolism, atherosclerosis, and insulin resistance, thereby contributing to the pathogenesis of non-alcoholic fatty liver disease. Conclusion: The mechanisms by which Artemisiae scopariae and Folium nelumbinis affect non-alcoholic fatty liver disease may involve multiple pathways, including insulin resistance, lipid metabolism, and atherosclerosis. This condition is characterized by numerous targets and a variety of active ingredients.