Exploring the Mechanism of Chen Pi in Treating Acute Ulcerative Colitis Based on Network Pharmacology and Molecular Docking

To investigate the mechanism of action of Chenpi in the treatment of acute ulcerative colitis, this experiment employed a combination of network pharmacology and molecular docking technology to make a preliminary prediction of its mechanism of action. The TCMSP and PubChem databases were employed to identify the active components of Chenpi and their respective targets. In contrast, the SwissTargetPrediction database was utilized to predict the potential targets of action of Chenpi. The relevant targets of acute ulcerative colitis were obtained from the GeneCards disease database and subsequently intersected with the targets of Chen Pi to identify the key targets of Chen Pi for the treatment of acute ulcerative colitis. The results of the network pharmacological analysis indicated that Chenpi may exert its effects through ESR1, potentially via the action of sitosterol, naringenin, 5,7-dihydroxy-2-(3-hydroxy-4-methoxyphenyl) chroman-4-one, Citromitin, and nobiletin, five active components, as well as PTGS2, PPARG, BCL2, SRC, and MMP9, and an additional 104 core targets. Following the enrichment analysis of the aforementioned 104 core targets, it was determined that pathways such as "Pathways in cancer," "Arachidonic acid metabolism," "Prostate cancer," "EGFR tyrosine kinase inhibitor resistance," and others were involved in the treatment of Chen Pi. The results of molecular docking also demonstrated that the active ingredients of Chen Pi exhibited favorable binding affinities with the key targets, thereby substantiating the precision of the network pharmacology-predicted outcomes. The results of this experiment suggest that Chenpi may exert its therapeutic effects on acute ulcerative colitis through a multi-component, multi-target, and multi-pathway mechanism.