Schisandrin A Suppresses Inflammation in DSS-induced IBD Mice and H₂O₂-induced MODE-K Cells through Wnt/β-Catenin Signaling

Abstract

Background Schisandrin A (SchA) has multiple pharmacological features, and inflammatory bowel disease (IBD) represents a common digestive system disease mainly characterized by inflammation. Objectives To assess the anti-inflammatory effects and the mechanism of SchA in mice with enteritis and in MODE-K cells representing in vivo and in vitro models of inflammation. Materials and Methods DSS-induced IBD mouse models and MODE-K cells (an in vitro model of the intestine) were used to assess the effects of SchA on IBD inflammation and to determine the related signaling pathways. Results Our data showed that SchA exerted anti-inflammatory effects by reducing the general clinical symptoms and the pathological damage to the colonic mucosa in mice with IBD and by promoting the migration of H2O2-induced MODE-K cells, inhibiting apoptotic death, and reducing the release of inflammatory factors. Moreover, SchA downregulated Wnt/β-catenin in both enteritis mice and H2O2-induced cells. Conclusion SchA inhibits inflammation in DSS-induced IBD mice and H2O2-induced MODE-K cells by repressing Wnt/β-catenin signaling.