![]() The impaired barrier function of the intestinal epithelium and dysregulated immune response in the intestinal mucosa play a key role in the pathogenesis of UC. UC is considered a global health problem with an accelerating incidence. Ulcerative colitis (UC) is a disease of unknown etiology characterized by inflammation of the mucosa and submucosa of the colon and rectum, leading to the development of ulcers. ![]() Our results suggest that SkQ1 may be a promising therapeutic agent for the treatment of inflammatory bowel diseases, in particular ulcerative colitis. Furthermore, C 12TPP did not prevent DSS-induced tight junction disassembly in Caco-2 cells. Pretreatment of mice by C 12TPP did not protect against DSS-induced colitis. SkQ1 prevented DSS-induced tight junction disassembly in Caco-2 cells. SkQ1 also reduced mRNA expression of pro-inflammatory molecules TNF, IL-6, IL-1β, and ICAM-1 in the proximal colon compared with DSS-treated animals. SkQ1 prevented the development of clinical and histological changes in DSS-treated mice. DSS-treated animals exhibited weight loss, bloody stool, dysfunction of the intestinal epithelium barrier (which was observed using FITC-dextran permeability), reduced colon length, and histopathological changes in the colon mucosa. ![]() ![]() The present work aimed to investigate the therapeutic potential of SkQ1 and C 12TPP, the analog of SkQ1 lacking the antioxidant quinone moiety, in the prevention of sodium dextran sulfate (DSS) experimental colitis and impairment of the barrier function of the intestinal epithelium in mice. The mitochondria-targeted antioxidant SkQ1, which is a derivative of plastoquinone, has been successfully used in preclinical studies for the treatment of cardiovascular and renal diseases, and has demonstrated anti-inflammatory activity in a number of inflammatory disease models. Mitochondria-targeted antioxidants have become promising candidates for the therapy of various pathologies. ![]()
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