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BMC Chemical Biology 2010
Dietary phenethylisothiocyanate attenuates bowel inflammation in miceAbstract: In two efficacy studies (acute and chronic) oral administration of PEO was effective at remitting acute and chronic signs of ulcerative colitis (UC) in mice. Disease activity, histology and biochemical characteristics were measured in the treated animals and were compared with appropriate controls. PEO treatment significantly improved body weights and stool consistency as well as decreased intestinal bleeding. PEO treatment also reduced mucosal inflammation, depletion of goblet cells and infiltration of inflammatory cells. Attenuation of proinflammatory interleukin1β production was observed in the colons of PEO-treated animals. Expression analyses were also carried out for immune function related genes, transcription factors and cytokines in lipopolysaccharide-activated mouse macrophage cells. PEO likely affects an intricate network of immune signaling genes including a novel concentration dependent reduction of total cellular Signal Transducer and Activator of Transcription 1 (STAT1) as well as nuclear phosphorylated-STAT1 (activated form of STAT1). A PEO-concentration dependent decrease of mRNA of C-X-C motif ligand 10 (a STAT1 responsive chemokine) and Interleukin 6 were also observed.PEO might be a promising candidate to develop as a treatment for ulcerative colitis patients. The disease attenuation by PEO is likely associated with suppression of activation of STAT1 transcription and inhibition of pro-inflammatory cytokines.Inflammatory bowel disease (IBD), affecting an estimated two million people annually in the US [1,2], is predominantly comprised of Crohn's disease (CD) and ulcerative colitis (UC). IBD is a set of chronic and relapsing inflammatory disorders of the intestine caused by multifactorial conditions in a genetically predisposed individual. UC primarily affects the mucosal lining of the colon and rectum, whereas CD may extend to any part of the gastrointestinal tract and is characterized by transmural inflammation [2,3]. Since the etiology of both
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