Objective: To explore the potential mechanism of action of levocarnitine in the treatment of epididymitis based on network pharmacology and experimental research.
Methods: The target proteins related to epididymitis and levocarnitine were retrieved through multiple databases, and the common targets were obtained using Venny software. The protein-protein interactions were obtained using the STRING database. Cytoscape software was used for visualization, and key targets were selected after topological analysis. GO and KEGG pathway enrichment analysis was performed using the DAVID database. Molecular docking was performed using Autodock Vina.
Results: A total of 130 drug targets and 2 151 disease targets were obtained, with 47 common targets. Protein-protein interaction network analysis identified core targets of levocarnitine in the treatment of epididymitis, including AKT1, HSP90AA1, ALB, CASP3, GSK3B, and GSR. KEGG pathway analysis suggested that metabolic pathways, lipid metabolism and atherosclerosis, cancer pathways, fluid shear stress and atherosclerosis, measles, chemical carcinogens-reactive oxygen species, purine metabolism, PI3K-Akt, and other signaling pathways may be associated with the mechanism of levocarnitine in the treatment of epididymitis.
Conclusion: This study revealed through network pharmacology that levocarnitine may act on multiple signaling pathways by targeting AKT1, HSP90AA1, ALB, CASP3, GSK3B, GSR, etc., thereby potentially exerting therapeutic effects on epididymitis.
Keywords: levocarnitine; epididymitis; network pharmacology; molecular docking technology.