Exploration of the Mechanism of Tripterygium Wilfordii in the Treatment of Myocardial Fibrosis Based on Network Pharmacology and Molecular Docking

Abstract

Background: A network pharmacology study on the biological action of tripterygium wilfordii on myocardial fibrosis（MF）. Methods: The effective components and potential targets of tripterygium wilfordii were screened from the TCMSP database to develop a combination target network. A protein-protein interaction network was constructed by analyzing the interaction between tripterygium wilfordii and MF, and then the Gene Ontology (GO) classification and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed. Furthermore, molecular docking was utilized to verify the results of the network analysis. Results: It was predicted that MF has 29 components that contribute to its effectiveness, as well as 87 potential targets. It is predicted that Tripterygium wilfordii has 29 active components and 87 potential targets for the treatment of MF. The principal active components of tripterygium wilfordii include kaempferol, β-sitosterol, triptolide, and Nobiletin. Signaling pathways: AGE-RAGE, PI3K-Akt, and MAPK may be involved in the mechanism of its action.7 Seven key targets (TNF, STAT3, AKT1, TP53, VEGFA, CASP3, STAT1) are possibly involved in the treatment of MF by tripterygium wilfordii. Conclusion: This study shows the complex network relationship between multiple components, multiple targets, and multiple pathways of Tripterygium wilfordii in treating MF.