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Exp Biol Med (Maywood). 2012 May;237(5):474-80. doi: 10.1258/ebm.2011.011358. Epub 2012 Mar 22.

Oxidative stress and redox signaling mechanisms of inflammatory bowel disease: updated experimental and clinical evidence.

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Laboratory of Molecular and Cellular Pharmacology and Toxicology, Department of Pharmacology, EVCOM, Virginia Tech Corporate Research Center RBII, Blacksburg, VA 24060, USA.


Inflammatory bowel disease (IBD) comprises primarily the chronic relapsing inflammatory disorders, Crohn's disease and ulcerative colitis, with the former affecting any part of the gastrointestinal tract and the latter mainly afflicting the colon. The precise etiology of IBD remains unclear, and it is thought that interactions among various factors, including genetic factors, the host immune system and environmental factors, cause disruption of intestinal homeostasis, leading to dysregulated inflammatory responses of the gut. As inflammation is intimately related to formation of reactive intermediates, including reactive oxygen and nitrogen species (ROS/RNS), oxidative stress has been proposed as a mechanism underlying the pathophysiology of IBD. This review is intended to summarize succinctly recent new experimental and clinical evidence supporting oxidative stress as a pathophysiological component of IBD and point to the potential of using antioxidant compounds as promising therapeutic modalities of human IBD. The sources of ROS/RNS and the redox signaling mechanism underlying oxidative stress and inflammation in IBD are discussed to provide insight into the molecular basis of oxidative stress as a pathophysiological factor in IBD.

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