beta-glucan suppresses LPS-stimulated NO production through the down-regulation of iNOS expression and NF kappa B Transactivation in RAW 264.7 macrophages

Abstract

The antioxidant and anti-inflammatory protective effects of beta-glucan from barley on RAW 264.7 murine macrophage cells induced by lipopolysaccharide (LPS) were examined. The RAW 264.7 murine macrophages were preincubated with various concentrations (0-200 mu g/mL) of beta-glucan and stimulated with LPS to induce oxidative stress and inflammation. The beta-glucan treatments were found to reduce thiobarbituric acid-reactive substance (TBARS) accumulation, and enhance glutathione levels and the activities of antioxidative enzymes, including superoxide dismutase (SOD), catalase, glutathione reductase, and glutathione peroxidase (GSH-px) in the LPS-stimulated macrophages as compared to the LPS-only treated cells. Nitric oxide (NO) production was significantly suppressed in a dose-dependent manner (p<0.05) with an IC50 of 104 mu g/mL. Further treatment with beta-glucan at 200 mu g/mL suppressed NO production to 2% of the LPS-control, and suppressed the levels of inducible nitric oxide synthase (NOS) protein and mRNA in a dose-dependent manner. The specific DNA binding activity of nuclear factor kappa B (NF kappa B) was significantly suppressed by beta-glucan treatment with an IC50 of 220 mu g/mL in a dose-dependent manner. Finally, barley beta-glucan ameliorates NO production and iNOS expression through the down-regulation of NF kappa B activity, which may be mediated by attenuated oxidative stress in RAW 264.7 macrophages.