The results of this study provide
an important insight into this issue. “
“Background and Aim: The term “stress-related mucosal disease” (SRMD) represents conditions ranging from superficial mucosal damage to focal deep mucosal damage in the stomach, of which pathogenesis is deduced to be violent mucosal ischemia or excess oxidative stress, but not fully clarified yet. Under the hypothesis that mucosal cell apoptosis subsequent to endoplasmic reticulum (ER) stress might play a crucial role, we evaluated the efficacy and mechanism that novel acid pump antagonist (APA), revaprazan, alleviated water immersion restraint stress (WIRS) induced SRMD in rats. Methods: In order to define whether WIRS-induced SRMD is associated with ER stress, we Osimertinib datasheet checked the alteration in the expression of ER stress markers including GRP78, CHOP, XBP-1, BiP as well as apoptosis in WIRS-induced SRMD. The efficacy
of revaprazan on either alleviating ER stress or attenuating SRMD was compared with proton pump inhibitor (PPI) and gastroprotectant. Results: Ten hours of WIRS induced a severe degree of SRMD, in which ER stress markers including CHOP, XBP1, and BiP were significantly overexpressed in the gastric tissues. However, these markers of ER stress were significantly decreased in the group pretreated with revaprazan compared to PPI or gastroprotectant, accompanied with a significant SB525334 mw reduction in apoptotic index. In addition to ER stress, revaprazan imposed anti-inflammatory benefit to limit SRMD based on significant levels of inflammatory cell apoptosis. Conclusion: PAK5 Endoplasmic reticulum stress accompanied with drastic apoptosis was implicated in the development of SRMD, but revaprazan could rescue the stomach from SRMD through alleviating ER stress in epithelial cells much better than either PPI or gastroprotectant. “
“See article in J. Gastroenterolol. Hepatol. 2011; 26: 1114–1122. Yoon et al.1 are to be congratulated on publishing the Korean experience of the clinical response to, and 1-year outcomes following, an initial
course of steroid therapy in ulcerative colitis (UC). While their data are not directly comparable to the series in the literature, due to variability in severity and referral patterns among studies, the results appear to be remarkably similar to what one sees in Western cohorts. In fact, the current data are highly reminiscent of one of the few studies mirroring their design.2 Following a cohort of 63 patients with UC treated with steroids between 1970 and 1993, Faubion et al. reported 1-year follow-up data. As one can appreciate, there are unlikely to be large, clinically-relevant differences in outcomes between these two cohorts (Table 1), especially when one applies a non-responder imputation to Yoon et al.’s1 data.
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