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.

Keywords: Schisandrin A; inflammatory bowel disease; MODE-K cell line; Wnt/β-catenin pathway