Highland barley β-glucan boosted intestinal epithelial regeneration via cell cycle and autophagy

Abstract

Cell cycle progression and autophagy take a crucial part in stimulating the regeneration of gut epithelial which definitely contributes to maintain the integrity of the intestinal barrier. Our previous research demonstrated that highland barley β-glucan (HBBG) significantly mitigated the damaged gastric mucosal and intestinal barrier of colitis mice, whenas the mechanism remains indistinct. In this study, we found that HBBG remitted the increase of disease activity index, the shortening of colon length and the damage of intestinal epithelial structure in mice with dextran sulphate sodium induced colitis. Furthermore, HBBG observably boosted gut epithelial regeneration on account of PCNA+ transit amplifying cells, Ki67+ crypt base columnar cells and goblet cells. Interestingly, HBBG relieved the apoptosis and suppressive proliferation of IEC-6 cells induced by lipopolysaccharide. The results of immunohistochemistry and flow cytometry demonstrated that HBBG promoted the cell cycle progression. Likewise, HBBG increased cell cycle related proteins CyclinD1 and CDK4 in IEC-6 cells. In the meanwhile, HBBG dramatically enhanced the autophagy. Excitingly, HBBG augmented the nuclear translocation of TFEB and phosphorylation of AMPK, which hinted HBBG activated autophagy via AMPK-TFEB signal. Expectantly, the treatment of 3-methyladenine, an autophagy inhibitor, inverted the promoted proliferation in IEC-6 cells caused by HBBG. Thereout, we presumed that HBBG accelerated the regeneration of intestinal epithelial by means of promoting cell cycle progression and activating the autophagy.