Coffea arabica pulp aqueous extract exhibits the anti-colitogenic effect in mice: preventive efficacy and possible mechanisms of action.

Inflammatory bowel disease (IBD) is a chronic inflammatory disease caused mainly by immune overactivation and intestinal mucosal barrier disruption. Coffea arabica pulp aqueous extract (CPE) contains a number of bioactive phenolic compounds that exhibit antioxidant and anti-inflammatory effects with previously unexplored application in experimental colitis. The aim of this study is to determine whether CPE produces anti-colitogenic effect and its possible mechanism of action. We found that CPE attenuated all IBD-related phenotypes and increased survival rates in dextran sulfate sodium (DSS)-induced colitis mice. In addition, CPE significantly suppressed mRNA and protein expression of myosin light-chain kinase (MLCK). Furthermore, CPE also inhibited MLCK recruitment to apical junction of colonic tissues of colitis mice. Although CPE had no effect on mRNA expression of tight junction genes, it reversed inflammation-mediated downregulation of ZO-1, occludin, and claudin-4 proteins in colitis mice. Importantly, CPE was able to recover ZO-1 and occludin localization to apical junction and suppressed tight junction-dependent leak pathway permeability in colitis mice. Indeed, CPE was also capable of stimulating sirtuin-1 (SIRT-1) in colonic tissues obtained from DSS-induced colitis mice, which is known to suppress inflammation and enhance intestinal barrier function. Therefore, SIRT-1 has been shown to be associated with CPE treatment in IBD model.