Uncovering the molecular mechanism of solasonine in treating interstitial cystitis via network pharmacology and molecular docking.

To search for potential targets and pathways of solasonine acting on Interstitial cystitis using network pharmacology and molecular docking methods, and to explore the potential mechanism of solasonine in the treatment of IC. Potential therapeutic targets of solasonine were retrieved from three databases: Pharmmapper, Targetnet, and SEA. GO and KEGG analyses were performed. IC-related genes were retrieved from the GEO and Genecards databases, and GO and KEGG analyses were performed. The STRING database combined with Cytoscape was used to map the protein interaction network (PPI) of IC-related targets and screen the core targets. The potential targets of solasonine and IC disease targets were intersected to obtain solasonine-IC common targets. Molecular docking techniques were utilized to confirm the binding of solasonine to primary targets. There are four common core targets of solasonine -IC, HMOX1, B2M, MUC1, and FAS, and molecular docking showed that solasonine binds stably to these four proteins. The analysis of these four gene pathways showed that solasonine regulated several inflammatory and cellular immune pathways, mainly involving the IL-18, apoptosis, and cytokine signaling pathway in the immune system. This study demonstrated that solasonine can inhibit polarization of M1 macrophages and M1-type inflammation. Solasonine may treat IC by targeting HMOX1, B2M, MUC1, FAS and affecting pathways such as the IL-18 signaling pathway, regulation of the apoptosis signaling pathway, and cytokine signaling pathways in the immune system.