Dietary oat β-glucan attenuates TNBS-induced colitis-associated hepatic redox and inflammatory disturbances via the gut-liver axis.

Abstract

Inflammatory bowel disease (IBD) frequently involves hepatobiliary complications linked to the gut-liver axis, yet dietary strategies targeting this pathway remain underexplored. We investigated the effects of dietary low-molar-mass oat β-glucan on hepatic redox balance and inflammatory cytokines in a rat model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Eighty-four male Sprague-Dawley rats were assigned to colitis or control groups, each fed a supplemented or non-supplemented diet for 3, 7, or 21 days. Hepatic total antioxidant status (TAS), lipid peroxidation (TBARS), superoxide dismutase (SOD), glutathione reductase (GR) and peroxidase (GPx) activities, and interleukin-1 (IL-1) and interleukin-6 (IL-6) concentrations were determined. In colitis animals, β-glucan progressively increased TAS and GR, maintained SOD at control levels, and reduced TBARS, GPx, IL-1, and IL-6, reaching control values by day 21. Under the tested conditions - a single low-molar-mass fraction (5.9 × 104 g/mol) at a single dietary level of 1% (w/w) - effects were time-dependent and inflammation-specific, with no modulation in healthy controls, supporting oat β-glucan of this molar mass as an adjunctive dietary strategy limiting extraintestinal hepatic complications of colitis. The dose- and molar-mass-dependence of the response remain to be established.