Β-Glucan Ameliorates Lps-Induced Inflammation and Barrier Injury Via Suppression of Tlr4/Nf-Κb Pathway in Iec-6 Cells

Abstract

This study aimed to investigate the protective effect of β-glucan on lipopolysaccharide (LPS)-induced inflammation in IEC-6 cells and its potential mechanisms. The cells were pretreated with β-glucan (30 μg/ml) for 12 h, and stimulated by LPS (20 μg/ml) for another 12 h. Compared with the control group, LPS administration resulted in decreased cell viability, intestinal barrier injury, increased cell apoptosis and inflammatory cytokines. These effects triggered by LPS were reversed by β-glucan pretreatment. In order to reveal the potential mechanisms, further exploration of the signaling pathway involved showed that β-glucan might inhibit the activation of toll like receptor 4 (TLR4)/NF-κB signaling pathway and increase the expression of tight junction proteins in LPS-induced IEC-6 cells. In conclusion, this finding suggested a protective effect of β-glucan in intestinal epithelial cells inflammation and indicated that β-glucan might be a potential therapeutic agent for the treatment of inflammatory intestinal diseases.

Keywords: β-glucan, lipopolysaccharide, tight junctions, Intestinal Barrier, TLR4-NF-κB