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Title 

Inhibition of cytokine-induced IκB kinase activation as a mechanism contributing to the anti-atherogenic activity of tilianin in hyperlipidemic mice

Authors 

K W NamJ KimJ J HongJ H ChoiW MarM H ChoY M KimSei Ryang OhHyeong Kyu LeeKi Hoan NamG T Oh

Publisher 

Elsevier

Issue Date 

2005

Citation 

Atherosclerosis, vol. 180, no. 1, pp. 27-35

Keywords 

atherosclerosiscytokineIKKtilianinflavonoidI kappa BI kappa B alphainterleukin 1lipopolysaccharidelipoprotein receptor

Abstract 

Tilianin has been shown to down-regulate TNF-α induced expression of vascular cell adhesion molecules in endothelial cells. In this study, we examined the anti-atherogenic effects and molecular mechanism of tilianin in vitro and in vivo. Male low-density lipoprotein receptor null mice (Ldlr-/-) fed a high cholesterol diet showed significant increases in the size of atherosclerotic lesions, as well as increased plasma levels of total cholesterol, triglycerides, and the pro-inflammatory cytokines TNF-α and IL-1β, when compared with Ldlr-/- mice fed a normal diet. Mice fed the high cholesterol diet supplemented with tilianin showed significantly reduced lesion sizes and reductions in cytokine levels, without significant changes in serum cholesterol levels. Primary cultured peritoneal macrophages from Ldlr-/- mice showed increased level of TNF-α andIL-1β mRNA in response to treatment with lipopolysaccharide; these increases were inhibited by co-treatment with tilianin. Moreover, tilianin inhibited NF-κB activation, as determined by electrophoretic mobility shift and NF-κB promoter assays. Upstream of NF-κB activation, tilianin inhibited IκB kinase activation and the subsequent phosphorylation and degradation of IκBα protein. These results suggest that tilianin ameliorates atherosclerosis by inhibiting the production of the NF-κB-dependent pro-inflammatory cytokines, TNF-α and IL-1β, via the inhibition of IκB kinase activity.

ISSN 

0021-9150

Link 

http://dx.doi.org/10.1016/j.atherosclerosis.2004.11.022

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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