5-Aminolevulinic acid (5-ALA) ameliorates DSS-induced colitis in mice via activation of the KEAP1-NRF2 signaling pathway
5-ALA directly inhibits the KEAP1-NRF2 interaction, enhances NRF2 nuclear translocation, and subsequently upregulates NRF2-mediated antioxidant responses, suppresses apoptosis and inflammation, and maintains mitochondrial function. These results highlight the therapeutic potential of 5-ALA in ulcerative colitis via the KEAP1-NRF2 pathway.