Abstract
This paper is focused on the role of reactive oxygen species (ROS), nitric oxide (NO), and carbon monoxide (CO) in inflammatory bowel disease. ROS and NO production as well as the expression of inducible NO synthase (iNOS) appears to be enhanced in the intestinal mucosa with active inflammation. Treatment of superoxide dismutase (SOD) or the potent iNOS inhibitor, ONO-1714, ameliorated colonic mucosal injury and NO production in mice administered with dextran sulfate sodium (DSS) in mice. The expression of heme oxygenase (HO)-1 is markedly induced in inflamed colonic tissue, and co-administration with an HO inhibitor enhanced inflammation and the disease activity index in mice. These results suggest that gaseous mediators may play a role in regulating the inflammatory response in the intestinal mucosa.
