ArticleDigestive diseases and sciences2008
CV-11974, angiotensin II type I receptor antagonist, reduces the severity of indomethacin-induced rat enteritis.
Article in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Angiotensin II inhibits P-glycoprotein in intestinal epithelial cells.Acta physiologica (Oxford, England) · 2020Article
- Blockade of the renin-angiotensin system prevents acute and immunologically relevant colitis in murine models.Pediatric surgery international · 2016Article
- Angiotensin converting enzyme-inhibitor reduces colitis severity in an IL-10 knockout model.Digestive diseases and sciences · 2013Article
- Use of enterally delivered angiotensin II type Ia receptor antagonists to reduce the severity of colitis.Digestive diseases and sciences · 2011Article
- Identification of dihalogenated proteins in rat intestinal mucosa injured by indomethacin.Journal of clinical biochemistry and nutrition · 2011Article
- Angiotensin II receptor expression and relation to Helicobacter pylori-infection in the stomach of the Mongolian gerbil.BMC gastroenterology · 2010Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
The aim of the present study was to examine the effect of angiotensin II type I receptor antagonist, CV-11974, on indomethacin-induced small intestinal injury in rats. Single administration of indomethacin provoked severe inflammatory lesions in the small intestine. The levels of thiobarbituric acid-reactive substances (TBARS), myeloperoxidase (MPO) activities and cytokine-induced neutrophil chemoattractant-1 (CINC-1) in the intestinal mucosa significantly increased in the indomethacin-treated group compared with the sham group. In addition, the angiotensin II type I receptor was increased in the small intestine after the administration of indomethacin. The development of intestinal lesions in response to indomethacin was prevented by pretreatment with CV-11974 together with significant suppression of the increased level of TBARS, MPO activities and CINC-1. These results indicate that CV-11974 protected against the small intestinal damage elicited by indomethacin, which suggests that angiotensin II/AT1 receptor interaction is involved in the pathogenesis of the intestinal inflammation associated with oxidative stress.
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