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Am J Physiol Cell Physiol 277: C403-C411, 1999;
0363-6143/99 $5.00
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Vol. 277, Issue 3, C403-C411, September 1999

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

Hirotsugu Kobuchi1, Sashwati Roy2,3, Chandan K. Sen1,2,3, Hao G. Nguyen2, and Lester Packer1,2

1 Environmental Energies Technologies Division, Lawrence Berkeley National Laboratory, and 2 Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; and 3 Department of Physiology, University of Kuopio, 70211 Kuopio, Finland

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 µM) manner. Quercetin had no effect on PMA- or TNF-alpha -induced nuclear factor-kappa B (NF-kappa B) 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.

flavonoids; intercellular adhesion molecule-1; activator protein-1; kinases; inflammation; c-Jun amino-terminal kinase


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