基于网络药理学及分子对接技术的川射干治疗咽喉炎机制研究

Investigation of Active Components for Pharyngitis Treatment Using Network Pharmacology and Molecular Docking Technology

目的:基于网络药理学和分子对接技术研究川射干治疗急慢性咽喉炎的作用机制,找出相应的化学成分,靶点蛋白及作用路径。方法:筛选川射干化学成分,采用uniprot数据库预测川射干作用靶点。以“laryngitis”为关键词检索咽喉炎相关靶点,并构建“活性成分-靶点”网络关系图。通过蛋白质相互作用分析,构建蛋白相互作用网络,进行通路富集分析,以探究川射干治疗咽喉炎的作用机制。结果:经筛选得到川射干5个良好的活性成分,预测到川射干治疗急慢性咽喉炎的主要靶点为谷胱苷肽S转移酶M1、细胞色素P4503A4酶、肿瘤坏死因子、细胞色素P450,家族2,亚家族A,肽6、冷感应蛋白、葡糖醛酸基转移酶1、醇脱氢酶6(V)、花生四烯酸5脂氧合酶、N-乙酰基转移酶2等。结论:研究得出川射干治疗急慢性咽喉炎作用潜在机制可能是β-谷甾醇、灰绿曲霉酰胺等成分与CASP3、JUN、GSTM1、CYP3A4、TNF等靶点调控多条信号通路发挥作用。

Objective:This study aimed to investigate the mechanisms of action in the treatment of acute and chronic pharyngitis using network pharmacology and molecular docking techniques,identifying the corresponding chemical components,target proteins,and action pathways.Methods:We collected and screened data from the UniProt database,using“laryngitis”as a keyword to retrieve pharyngitis-related targets.A network diagram of“active ingredient-target”was constructed.Through protein interaction analysis,we established a protein interaction network and conducted pathway enrichment analysis to explore the mechanisms underlying pharyngitis.Results:After screening,we identified five key active components and predicted 20 potential targets for treating acute and chronic pharyngitis.The main targets for the treatment of pharyngitis included glutathione Stransferase M1,cytochrome P4503A4,tumor necrosis factor,cytochrome P450 family 2 subfamily A6,cold-sensing protein,glucuronosyltransferase 1,alcohol dehydrogenase 6(V),arachidonate 5-lipoxygenase,and N-acetyltransferase,among others.GO analysis and KEGG pathway analysis indicated that the signaling pathways associated with acute and chronic pharyngitis primarily involved lipid and atherosclerosis pathways,human cytomegalovirus infection pathways,hepatitis B pathways,and AGE-RAGE signaling pathways.Cconslusion:The potential mechanisms of treatment for acute and chronic pharyngitis may involve the regulation of multiple signaling pathways,such as CASP3,JUN,GSTM1,CYP3A4,and TNF,through the action ofβ-sitosterol and its components.