Erschienen in:
01.09.2010 | Original Research Paper
Cyanidin-3-O-β-glucoside inhibits LPS-induced expression of inflammatory mediators through decreasing IκBα phosphorylation in THP-1 cells
verfasst von:
Yinghui Zhang, Fuzhi Lian, Yanna Zhu, Min Xia, Qing Wang, Wenhua Ling, Xiang-Dong Wang
Erschienen in:
Inflammation Research
|
Ausgabe 9/2010
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Abstract
Objective and design
As a common phytochemical, cyanidin 3-O-β-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 TNFα 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 μM) in the absence or presence of 1 ng/mL LPS. mRNA expression levels were detected by real time PCR, and secretion of TNFα and IL-6, phosphorylated IκBα, and nuclear factor-kappa B (NF-κB) P65 were monitored by ELISA or Western blotting analysis. The role of an inhibitor of IκBα phosphorylation, BAY 11-7082, in C3G inhibition of LPS-induced cytokines expression was investigated.
Results
C3G (0.05–0.5 μM) treatment significantly inhibited LPS-stimulated TNFα and IL-6 mRNA expression and secretion of these proteins by THP-1 cells. Phosphorylation of IκBα and NF-κB nuclear translocation could be blocked by 0.5 μM C3G. BAY 11-7082 treatment abolished C3G-induced reduction of TNFα and IL-6.
Conclusion
Our results suggest that C3G exerts its anti-inflammatory effect through inhibiting IκBα phosphorylation, thereby suppressing NF-κB activity in THP-1 cells.