OBJECTIVE AND DESIGN: 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 TNFalpha and IL-6 expression in the human monocyte/macrophage cell line THP-1, and to explore the mechanisms involved. METHODS: Differentiated THP-1 cells were treated with different concentrations of C3G (0.005, 0.05, 0.5,10 microM) in the absence or presence of 1 ng/mL LPS. mRNA expression levels were detected by real time PCR, and secretion of TNFalpha and IL-6, phosphorylated IkappaBalpha, and nuclear factor-kappa B (NF-kappaB) P65 were monitored by ELISA or Western blotting analysis. The role of an inhibitor of IkappaBalpha phosphorylation, BAY 11-7082, in C3G inhibition of LPS-induced cytokines expression was investigated. RESULTS: C3G (0.05-0.5 microM) treatment significantly inhibited LPS-stimulated TNFalpha and IL-6 mRNA expression and secretion of these proteins by THP-1 cells. Phosphorylation of IkappaBalpha and NF-kappaB nuclear translocation could be blocked by 0.5 microM C3G. BAY 11-7082 treatment abolished C3G-induced reduction of TNFalpha and IL-6. CONCLUSION: Our results suggest that C3G exerts its anti-inflammatory effect through inhibiting IkappaBalpha phosphorylation, thereby suppressing NF-kappaB activity in THP-1 cells.
OBJECTIVE AND DESIGN: 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 TNFalpha and IL-6 expression in the human monocyte/macrophage cell line THP-1, and to explore the mechanisms involved. METHODS: Differentiated THP-1 cells were treated with different concentrations of C3G (0.005, 0.05, 0.5,10 microM) in the absence or presence of 1 ng/mL LPS. mRNA expression levels were detected by real time PCR, and secretion of TNFalpha and IL-6, phosphorylated IkappaBalpha, and nuclear factor-kappa B (NF-kappaB) P65 were monitored by ELISA or Western blotting analysis. The role of an inhibitor of IkappaBalpha phosphorylation, BAY 11-7082, in C3G inhibition of LPS-induced cytokines expression was investigated. RESULTS:C3G (0.05-0.5 microM) treatment significantly inhibited LPS-stimulated TNFalpha and IL-6 mRNA expression and secretion of these proteins by THP-1 cells. Phosphorylation of IkappaBalpha and NF-kappaB nuclear translocation could be blocked by 0.5 microM C3G. BAY 11-7082 treatment abolished C3G-induced reduction of TNFalpha and IL-6. CONCLUSION: Our results suggest that C3G exerts its anti-inflammatory effect through inhibiting IkappaBalpha phosphorylation, thereby suppressing NF-kappaB activity in THP-1 cells.
Authors: F Mercurio; H Zhu; B W Murray; A Shevchenko; B L Bennett; J Li; D B Young; M Barbosa; M Mann; A Manning; A Rao Journal: Science Date: 1997-10-31 Impact factor: 47.728
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