The Alleviating Effects and Mechanisms of Betaine on Dextran Sulfate Sodium-Induced Colitis in Mice

Scope: Ulcerative colitis (UC) is an intestinal disease that is becoming increasingly prevalent and is often overlooked in early stages, and its pathogenesis is often closely related to inflammatory processes. Betaine is a natural product with anti-inflammatory effects that exists in a wide range of plants and animals.Methods and results: In this study, the protective effects of betaine are investigated on intestinal barrier function in a mouse model, a dextran sulfate sodium-induced ulcerative colitis and its mechanism of action in the inflammatory context. FITC-dextran 4000 Da (FD-4) flux, disease activity index, histopathological scores, and inflammatory factor levels in sera are determined across different groups. In addition, Caco-2 cell monolayer barrier function is evaluated by transepithelial resistance and FD-4 flux. The expression levels and distribution of tight junction proteins are determined using Western blot and immunofluorescence, respectively. Activation of the NF-kappa Bp65/MLCK/p-MLC signaling pathway is detected by Western blot. Chromatin immunoprecipitation is performed to examine the binding of NF-kappa B to the MLCK gene promoter. The results indicated that betaine inhibits NF-kappa B-mediated activation of the MLCK/p-MLC signaling pathway to protect the intestinal barrier function of mice with UC.Conclusion: Betaine can be used as a potential candidate drug to improve intestinal barrier dysfunction in patients with UC.

Automated summary

This study investigates the protective effects of betaine on intestinal barrier function in a mouse model of ulcerative colitis and reveals its mechanism of action. The results show that betaine protects the intestinal barrier function of mice with ulcerative colitis by inhibiting the activation of the NF-kappa B-mediated signaling pathway.