Green tea extract and Piper retrofractum attenuate deoxycholic acid-induced damage and enhance the tight junction barrier: An analysis in a Caco-2 cell culture model and a DSS coinduced mouse model

Abstract

This study investigated the effect of green tea extract (GTE) and green tea–Piper retrofractum complex (GPX), on tight junctions (TJs) in a cellular model of deoxycholic acid (DCA)-induced intestinal barrier disruption and a mouse DSS + DCA-induced colitis model. Green tea and P. retrofractum were extracted and coadministered to examine the bioavailability and effects of combined catechins and piperine on colonic TJ damage. The ability of GPX to alleviate TJ damage was determined by comparing the transepithelial electrical resistance (TEER), FITC-dextran flux, and mRNA expression of TJ-related components and target expression pathway in the GTE and GPX groups. Compared with the DCA-treated group, the GTE- and GPX-treated groups showed significantly enhanced TEER, FITC-dextran flux, and TJ-related mRNA expression (p < 0.05). Cell treatment also downregulated the mRNA encoding bile acid receptor and decreased ERK1/2 phosphorylation. Compared with the GTE-treated group, the GPX-treated group showed higher mRNA expression of zonula occludens-1, occludin, claudin-3, and claudin-4; greater restoration of TJs, as determined by immunofluorescence; and better modulation of ERK1/2 activation. In the in vivo model, GPX-pretreated mice showed an improved intestinal damage index and colon length compared with mice in the other colitis-induced groups. Both extracts recovered the distal colon mRNA expression of zonula occludens-1 and claudin-1. These results suggest that GTE improves intestinal health by protecting TJs from secondary bile acid damage and that P. retrofractum may potentiate the bioactivity of green tea catechins.