Ulcerative colitis (UC) is a chronic inflammatory disease with an unclear pathogenesis. This study aimed to investigate the therapeutic mechanism of leonurine in UC. Using network pharmacology and bioinformatics analysis, we identified the PINK1/Parkin-mediated mitophagy pathway as a key target. Validation in a DSS-induced colitis mice model showed that leonurine significantly alleviated colonic injury, reduced inflammatory cytokines, and restored intestinal barrier function. Mechanistically, leonurine upregulated the expression of mitophagy-related proteins (PINK1, Parkin, LC3II) and improved mitochondrial morphology. In conclusion, leonurine ameliorates UC by activating the PINK1/Parkin-mediated mitophagy pathway, providing a scientific basis for its development as a potential therapeutic agent.
Cao et al. (Thu,) studied this question.