Quercetin inhibits inducible ICAM-1 expression in human endothelial cells through the JNK pathway

被引:150
作者
Kobuchi, H
Roy, S
Sen, CK
Nguyen, HG
Packer, L
机构
[1] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[2] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Environm Energies Technol Div, Berkeley, CA 94720 USA
[3] Univ Kuopio, Dept Physiol, FIN-70211 Kuopio, Finland
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1999年 / 277卷 / 03期
关键词
flavonoids; intercellular adhesion molecule-1; activator protein-1; kinases; inflammation; c-Jun amino-terminal kinase;
D O I
10.1152/ajpcell.1999.277.3.C403
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Quercetin inhibits inducible ICAM-1 expression in human endothelial cells through the JNK pathway. Am. J. Physiol. 277 (Cell Physiol. 46): C403-C411, 1999.-The cell adhesion molecule intercellular adhesion molecule-1 (ICAM-1) plays a pivotal role in inflammatory responses. Quercetin (3,3',4',5,7-pentahydroxyflavone), a naturally occurring dietary flavonol, has potent anti-inflammatory properties. The effect of quercetin on ICAM-1 expression induced by agonists phorbol 12-myristate 13-acetate (PMA) and tumor necrosis factor-alpha (TNF-alpha) in human endothelial cell line ECV304 (ECV) was investigated. Quercetin treatment downregulated both PMA- and TNF-alpha-induced surface expression, as well as the ICAM-1 mRNA levels, in ECV cells in a dose-dependent (10-50 l-IM) manner. Quercetin had no effect on PMA- or TNF-alpha-induced nuclear factor-KB (NF-KB) activation. However, under similar conditions a remarkable dose-dependent downregulation of activator protein-1 (AP-1) activation was observed. This decrease in AP-1 activation was observed to be associated with the inhibitory effects of quercetin on the c-Jun NH2-terminal kinase (JNK) pathway. These results suggest that quercetin downregulates both PMA- and TNF-alpha-induced ICAM-1 expression via inhibiting both AP-1 activation and the JNK pathway.
引用
收藏
页码:C403 / C411
页数:9
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