Authors
Esraa G El-Waseif, Manar A Nader, Aamal G El-Waseif, Marwa E Abdelmageed
Published in
European journal of pharmacology. Pages 179481. Oct 26, 2026. Epub Oct 26, 2026.
Abstract
Ulcerative colitis (UC); as one of the inflammatory bowel diseases (IBD), arises from chronic inflammation of the intestinal tract. In this study, we addressed the possible protective mechanisms of vonoprazan, as a potassium-competitive acid blocker, on dextran sulfate sodium (DSS)-mediated UC. Therefore, male BALB-c mice administered oral vonoprazan (10 or 20 mg/kg/day) for 10 days and received drinking water containing 3% w/v DSS for 7 days from day 4. Vonoprazan exhibited a promising effect against UC by increasing mice body weight, colon length, and spleen weight, decreasing serum C-reactive protein (CRP) concentration and the disease activity index (DAI), and alleviating colonic histopathological changes. Colonic tissue antioxidants increased significantly in vonoprazan-treated groups. Additionally, colonic tissue oxidative stress was significantly ameliorated in vonoprazan-treated mice. Furthermore, vonoprazan preserved the integrity of intestinal mucosal barrier function and attenuated UC by decreasing the levels of immuno-inflammatory cells, inflammation-related proteins, and pro-inflammatory cytokines, elevating the tight junction proteins levels, and ameliorating mitochondrial energy metabolism. Taken together, vonoprazan protected against DSS-mediated UC in mice via antioxidant and anti-inflammatory activities that maintained tight junction architecture.
PMID:
42933761
Bibliographic data and abstract were imported from PubMed on 27 Oct 2026.
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