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Erschienen in: Inflammation Research 9/2010

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.
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Metadaten
Titel
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
Publikationsdatum
01.09.2010
Verlag
SP Birkhäuser Verlag Basel
Erschienen in
Inflammation Research / Ausgabe 9/2010
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-010-0183-7

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