基于网络药理学的人参特殊成分治疗溃疡性结肠炎的现代药理机制探讨

Weichen Si
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摘要

背景与目的:利用网络药理学方法探讨人参特殊成分治疗溃疡性结肠炎的主要作用靶点、关键通路及其作用机制。为后续实验室实验和临床试验提供理论依据。方法:通过TCMSP数据库获得三七的主要有效成分,并进行特异性成分筛选。三七特异性成分的靶标来源于瑞士靶标预测数据库。使用GeneCards、OMIM和DisGent数据库获得与溃疡性结肠炎相关的靶标。利用STRING数据库构建了相交靶点的蛋白相互作用网络(PPI)。在R语言软件中进行GO函数和KEGG通路富集分析。利用Cytoscape软件构建了中草药-成分-靶点-疾病- kegg通路网络。结果:获得了三七的7种主要有效成分,其中人参皂苷f2为一种特殊成分,对应16个潜在靶点。对疾病数据库的搜索产生了5536个溃疡性结肠炎的靶点。通过交叉靶点蛋白相互作用分析获得8个核心靶点:STAT3、VEGFA、HSP90AA1、FGF2、IL2、MET、BCL2L1和RORC。GO功能富集分析得到417条通路,KEGG富集分析得到22条具有统计学意义的通路。结论:人参皂苷f2治疗溃疡性结肠炎的作用机制具有多靶点、多途径相互作用的特点。受体可能与STAT3、VEGFA、HSP90AA1、FGF2、IL2、MET等靶点相关,主要信号通路可能与PI3K-Akt信号通路、Th17细胞分化、炎症性肠病等相关,为下一步深入实验研究提供理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exploring the Modern Pharmacological Mechanism of Special Ingredients of Panax Ginseng for Ulcerative Colitis based on Network Pharmacology
Background and Objective: To explore the main action targets and key pathways, along with their mechanisms of action, of Panax ginseng’s special ingredients in the treatment of ulcerative colitis using network pharmacology methods. To provide a theoretical basis for subsequent laboratory experiments and clinical trials. Methods: The main active ingredients of Panax notoginseng were obtained through the TCMSP database and the specific ingredients were screened. The targets of Panax notoginseng-specific components were obtained from the Swiss Target Prediction database. The GeneCards, OMIM, and DisGent databases were used to obtain the targets related to ulcerative colitis. The protein interaction network (PPI) of intersecting targets was constructed using the STRING database. GO function and KEGG pathway enrichment analysis were performed in R language software. Construction of the herb-component-target-disease-KEGG pathway network was achieved using Cytoscape software. Results: Seven major active ingredients of Panax notoginseng were obtained, and ginsenoside f2 was found to be a special ingredient, corresponding to 16 potential targets. A search of the disease database yielded 5,536 targets for ulcerative colitis. Eight core targets were obtained by protein interaction analysis of the intersecting targets: STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, BCL2L1, and RORC, respectively. 417 entries were obtained by GO functional enrichment analysis, and 22 statistically significant pathways were obtained by KEGG enrichment analysis. Conclusion: The mechanism of action of ginsenoside f2 in the treatment of ulcerative colitis features multi-target and multi-pathway interactions. The receptors may be related to STAT3, VEGFA, HSP90AA1, FGF2, IL2, MET, and other targets, and the main signaling pathways may be related to the PI3K-Akt signaling pathway, Th17 cell differentiation, and inflammatory bowel disease among others and this provides a theoretical basis for the next in-depth experimental study.
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