基于网络药理学和分子对接探讨青蒿防治2型糖尿病的作用机制研究

Study on the Mechanism of Artemisia Annua in Prevention and Treatment of Type 2 Diabetes Mellitus Based on Network Pharmacology and Molecular Docking

摘要: 目的：通过网络药理学和分子对接初步揭示了青蒿抗2型糖尿病的作用机制。方法：从中药系统药理学数据库与分析平台(TCMSP)中根据OB值和DL值选出青蒿的有效成分和成分所对应的靶点，取青蒿和2型糖尿病的交集基因做PPI蛋白互作网络图，通过David数据库进行基因本体(GO)和京都基因与基因组百科全书(KEGG)分析，最后采用分子对接验证。结果：筛选得到青蒿的活性成分22个、交集基因163个，通过蛋白互作分析发现“JUN、TP53、AKT1”治疗2型糖尿病的作用，KEGG富集发现，可能通过pathways in cancer、AGR-GAGE signaling pathway in diabetic complications、Lipid and atherosclerosis等信号通路进行调控。分子对接结果表明青蒿中的EUPATIN、isorhamnetin、sitosterol等活性成分与“JUN、TP53、AKT1”有非常强的结合能力。结论：青蒿可能是通过EUPATIN、isorhamnetin、sitosterol等成分调控pathways in cancer等相关信号通路上的JUN、TP53、AKT1等基因发挥治疗2型糖尿病的作用。

Abstract: Objective: To preliminarily reveal the mechanism of action of Artemisia annua against type 2 dia-betes mellitus through network pharmacology and molecular docking. Methods: The active ingre-dients and corresponding targets of Artemisia annua were selected from the pharmacology data-base and analysis platform (TCMSP) of the Chinese medicine system according to the OB value and DL value, the intersection genes of Artemisia annua and type 2 diabetes mellitus were taken as PPI protein interaction network diagram, and the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed through the David database, and finally the molecular docking was used for verification. Results: 22 active ingredients and 163 intersecting genes of Artemisia annua were screened, and the effect of “JUN, TP53 and AKT1” in the treatment of type 2 diabetes was found by protein interaction analysis, and KEGG enrichment was found, which may be regulated through pathways in cancer, AGR-GAGE signaling pathway in diabetic complications, Lipid and Signaling pathways such as atherosclerosis. The molecular docking results show that the active ingredients such as EUPATIN, isorhamnetin and sitosterol in Artemisia annua have a very strong binding ability with “JUN, TP53 and AKT1”. Conclusion: Artemisia annua may play a role in the treatment of type 2 diabetes mellitus by regulating JUN, TP53, AKT1 and other genes in related signaling pathways such as EUPATIN, isorhamnetin, sitosterol and other components.