Network pharmacology and molecular docking-based investigation on the mechanisms of action of Coptidis Rhizoma in the treatment of gastric precancerous lesions

Abstract

Abstract Background Gastric precancerous lesions are a critical stage in the development of gastric cancer or gastric adenocarcinoma, and their outcome plays an important role in the malignant progression of gastric cancer. Coptidis Rhizoma has a good effect on Gastric precancerous lesions. However, its specific mechanism of action remains incompletely elucidated. Methods A network pharmacology and molecular docking techniques were used to explore the active ingredients and molecular mechanism of Coptidis Rhizoma in treating gastric precancerous lesions. The active compounds of Coptidis Rhizoma and their potential gastric precancerous lesions related targets were obtained from TCMSP, GeneCards, and OMIM databases. An interaction network based on protein-protein interactions (PPIs) was constructed to visualize the interactions between hub genes. Analysis of GO enrichment and KEGG pathway were conducted using the DAVID database. An investigation of interactions between active compounds and potential targets was carried out by molecular docking. Results A total of 11 active compounds and 95 anti gastric precancerous lesions targets of Coptidis Rhizoma were screened for analysis. GO enrichment analysis showed that the mechanism of Coptidis Rhizoma acting on precancerous gastric lesions involved in gene expression regulation and apoptosis regulation. KEGG pathway enrichment analysis showed that Coptidis Rhizoma against precancerous gastric lesions involving the MAPKsignalling pathway and PI3K/AKT signalling pathway. Molecular docking simulations indicated potential interactions between these compounds (quercetin, palmatine, berberine, berberrubine) and targets (EGFR, AKT1, MYC, TP53) involved in anti gastric precancerous lesions activity. conclusion Bioactive compounds in Coptidis Rhizoma have the potential to prevent atrophy and intestinal metaplasia.These compounds function by regulating the proteins implicated in MAPK and PI3K/AKT signalling pathways that are crucial in gastric epithelial cell differentiation, proliferation and maturation.