RESUMEN
BACKGROUND: Atherosclerosis (AS) is the cause of most cardiovascular diseases and imposes a huge economic burden on society. Erchen decoction (ECD) is an effective formula for treating AS, but its therapeutic mechanism remains unclear. This study will explore the mechanism of ECD mechanism for treating AS using network pharmacology and molecular docking. METHODS: We searched ECD chemical composition information and related targets via Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform and SwissTargetPrediction databases, and gene names correction was performed using the UniProt database. AS-related targets were retrieved from OMIM, GeneCards, and DrugBank databases, and Venny 2.1 were used for intersection analysis. Protein-protein interaction network was constructed by the STRING database, and an interactive network of the drug-component-target-disease was drawn using the Cytoscape 3.9.0 software. Gene ontology and Kyoto Gene and Genome Encyclopedia enrichment analysis were performed by the DAVID database, and molecular docking validation of vital active ingredients and action targets of ECD was performed using AutoDock Vina software. RESULTS: The 127 active components of ECD act on AS by regulating 231 targets and 151 pathways. The 6 core components are quercetin, polyporenic acid C, 18α-hydroxyglycyrrhetic acid, glyuranolide, 3beta-hydroxychloroxy-24-methylene-8-lanostene-21-oic acid, and obacunone. They may regulate AS by regulating core target genes, such as JUN, SRC, AKT1, PTGS2, ESR1, AR, MAPK1, MAPK3, and RELA, and acting on multiple vital pathways, such as AGE-RAGE signaling pathway in diabetic complications, Lipid and AS, and Fluid shear stress and AS. Molecular docking showed that the selected target protein had good binding activity to the active ingredient. CONCLUSIONS: ECD has the characteristics of multi-components, multi-targets and multi-pathways in the treatment of AS. The results provide a theoretical basis for the clinical application of ECD and its mechanism.