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This is consistent with previous findings that -cell plasticity occurs in common forms of -cell dysfunction, and is caused by the downregulation of FoxO1 that follows hyperglycemia-induced oxidative stress 26

doi: 10.1136/gut.30.4.436

Since the redox status of mucosal glutathione is associated with inflammation and disease progression, impaired mucosal antioxidant defenses likely contribute to the development of UC ( Chronic NF-B stimulation promotes cellular infiltration and mucosal inflammation by increasing the transcription of proinflammatory cytokines (e.g., IL-6, IL-8, IL-16, and TNF-) and by degrading the intestinal barrier through increased apoptosis of intestinal epithelial cells ( Figure 3 ) ( Figure 3 One of the well-established signaling pathways that play a vital role in the modulation of mucosal immunological tolerance relevant to the pathogenesis of IBD is the Janus kinase/signal transducer and activator of transcription (JAK/STAT) system ( TGF- , TNF- , IL-2 , IL-6 , IL-8 , MMP9 , Intercellular Adhesion Molecule 1 ( ICAM-1 / CD54 ), STAT1 , and STAT3 ) ( 6 Role of antioxidants for IBD-related therapeutic applications and hormonal intervention Oxidative/nitrosative stress is a significant pathophysiologic factor that plays a role in the initiation and progression of IBD