Cyanidin-3-O-β-glucoside inhibits LPS-induced expression of inflammatory mediators through decreasing IκBα phosphorylation in THP-1 cells

As a common phytochemical, cyanidin 3-O-beta-glucoside (C3G) has a role in inhibiting inflammatory mediators; however, its mechanism of action remains unclear. The purpose of this study was to explore the effect of C3G on lipopolysaccharide (LPS)-stimulated TNF alpha and IL-6 expression in the human monocyte/macrophage cell line THP-1, and to explore the mechanisms involved. Differentiated THP-1 cells were treated with different concentrations of C3G (0.005, 0.05, 0.5,10 mu M) in the absence or presence of 1 ng/mL LPS. mRNA expression levels were detected by real time PCR, and secretion of TNF alpha and IL-6, phosphorylated I kappa B alpha, and nuclear factor-kappa B (NF-kappa B) P65 were monitored by ELISA or Western blotting analysis. The role of an inhibitor of I kappa B alpha phosphorylation, BAY 11-7082, in C3G inhibition of LPS-induced cytokines expression was investigated. C3G (0.05-0.5 mu M) treatment significantly inhibited LPS-stimulated TNF alpha and IL-6 mRNA expression and secretion of these proteins by THP-1 cells. Phosphorylation of I kappa B alpha and NF-kappa B nuclear translocation could be blocked by 0.5 mu M C3G. BAY 11-7082 treatment abolished C3G-induced reduction of TNF alpha and IL-6. Our results suggest that C3G exerts its anti-inflammatory effect through inhibiting I kappa B alpha phosphorylation, thereby suppressing NF-kappa B activity in THP-1 cells.