ArticleFolia microbiologica2026
Tegoprazan regulates gut microbiota structure in Helicobacter pylori-induced ulcerative colitis mice.
Article in Folia microbiologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Helicobacter pylori (H. pylori) infection promotes pathogenesis of ulcerative colitis (UC). Tegoprazan, as the firs-line therapy for H. pylori eradication, alleviates inflammatory bowel disease. This study aimed to investigate the effects of Tegoprazan on UC. Helicobacter pylori (H. pylori) infection was performed to establish a mouse UC model. Histological analysis was conducted using HE staining and Alcian blue-periodic acid Schiff staining. Gene expression was detected using Western blot and RT-qPCR. Cytokine levels were analyzed using ELISA. Cell apoptosis was analyzed using TUNEL. Gut microbiota structure was analyzed using 16s rRNA sequencing. Tegoprazan alleviated H. pylori infection-induced the destruction of the crypt structure and intestinal barrier structure. Moreover, Tegoprazan inhibited the inflammatory response and the death of goblet cells. Moreover, gut microbiota achieved a new equilibrium state. Teg mediated the eradication of H. pylori and the release of short-chain fatty acids. Taken together, Tegoprazan protects against the progression of UC through regulating gut microbiota and regulating fatty acid metabolism, improving intestinal mucosal barrier integrity. Clinical trial: not applicable.
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