Sulfide Quinone Oxidoreductase Alleviates Acute Ulcerative Colitis by Regulating Mitochondrial Dysfunction.

Alteration in mitochondrial function within intestinal epithelial cells were closely related to inflammatory bowel disease (IBD) progression. Sulfide quinone oxidoreductase (), located in the inner mitochondria membrane, is a crucial enzyme in sulfide metabolism. Here, we observed that was downregulated during colitis. Intestinal epithelial cells specific knockout of ( ) mice were more susceptible to acute ulcerative colitis (UC) with lower hydrogen sulfide (HS) levels, and the absence of caused a breakdown of the epithelial barrier through disruption of the tight junction proteins. Furthermore, analysis of the mitochondrial morphology and functions revealed increased mitochondrial damage when deficiency. Mechanistically, it is observed that knockout increased lipid peroxidation, malondialdehyde (MDA) levels and ferroptosis. Further results demonstrated that may rely on inhibiting excessive mitochondrial division and promoting mitochondrial biogenesis to regulate reaction oxygen species (ROS) levels in intestinal epithelial cells. Treatment with ROS scavengers (NAC) showed significant reduced colonic inflammation symptoms observed in DSS-treated mice. Collectively, these findings demonstrate the protective role of in intestinal epithelial cells in maintaining mitochondrial homeostasis by regulating ROS and providing novel insight into UC.