Tegoprazan regulates gut microbiota structure in Helicobacter pylori-induced ulcerative colitis mice
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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