Abstract
Background: In this study, we investigate the impact of epigallocatechin gallate (EGCG), the most abundant and potent catechin in green tea, on a mouse model of inflammatory bowel disease (IBD) and the underlying mechanisms of action. Methods: C57BL/6J mice were subjected to dextran sulfate sodium (DSS)-induced IBD-like disease and then randomly divided into three groups: Model group (MD), low-dose EGCG group (LE, 20 mg/kg/d), and high-dose EGCG group (HE, 50 mg/kg/d). DSS-induced clinical and macroscopic changes were monitored daily. Intestinal permeability was assessed by FITC-Dextran assay. Results: Both high- and low-dose EGCG treatment alleviated clinical manifestations including body weight loss and disease activity index (DAI) of DSS-induced colitis. The DAI score was significantly improved after two days of EGCG treatment. At the end of the study, the macroscopic severity score (MSS) of HE and LE treatment groups were 2.4 ± 1.2, and 2.2 ± 1.0, respectively, significantly lower than that of the controls (5.0 ± 2.1). EGCG treatment also prevented colon shortening, and improved intestinal permeability and histopathological changes. In addition, EGCG treatment attenuated colon inflammation by suppressing colonic levels of pro-inflammatory cytokines IL-6, MCP-1, and TNF-alpha, and inhibited CD3+ T cell and CD68+ macrophage infiltration. Conclusion: EGCG is effective in inflammatory colitis because it reduces cellular and molecular inflammation, and reduces intestinal permeability.
Highlights
Inflammatory bowel disease (IBD) is an autoimmune disease, which involves chronic inflammation of different parts of the gastrointestinal tract resulting from an inappropriate mucosal immune response to intestinal microbes [1]
epigallocatechin gallate (EGCG) is effective in inflammatory colitis because it reduces cellular and molecular inflammation, and reduces intestinal permeability
The pathogenesis of inflammatory bowel disease (IBD) has not been fully elucidated, it is widely accepted that genetic susceptibility and environmental factors induce impairment of mucosal barrier function and translocation of intestinal microbes, which in turn, leads to the activation of both innate and adaptive immune system and production of cytokines resulting in tissue injury and clinical manifestations [1,3]
Summary
Inflammatory bowel disease (IBD) is an autoimmune disease, which involves chronic inflammation of different parts of the gastrointestinal tract resulting from an inappropriate mucosal immune response to intestinal microbes [1]. The pathogenesis of IBD has not been fully elucidated, it is widely accepted that genetic susceptibility and environmental factors induce impairment of mucosal barrier function and translocation of intestinal microbes, which in turn, leads to the activation of both innate and adaptive immune system and production of cytokines resulting in tissue injury and clinical manifestations [1,3]. Results: Both high- and low-dose EGCG treatment alleviated clinical manifestations including body weight loss and disease activity index (DAI) of DSS-induced colitis. EGCG treatment attenuated colon inflammation by suppressing colonic levels of pro-inflammatory cytokines IL-6, MCP-1, and TNF-alpha, and inhibited CD3+ T cell and CD68+ macrophage infiltration
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