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INHIBITION OF NF–KB AND STAT3 BY QUERCETIN WITH SUPPRESSION OF ADHESION MOLECULE EXPRESSION IN VASCULAR ENDOTHELIAL CELLS

YOUNG-SUK CHO ^1#, CHAN HYUNG KIM ^1#, TAE–SUN HA ², HEE YUL AHN ^1*

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Intercellular adhesion molecule 1 (ICAM–1), vascular cell adhesion molecule 1 (VCAM–1), P– and E–selectin play a key role for the initiation of vascular inflammation. In this study, we explored the mechanism by which quercetin may inhibit ICAM–1 and VCAM–1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVEC). Quercetin prevented LPS–mediated increase of ICAM–1 and VCAM–1 expression. Stattic (6-Nitrobenzo[b]thiophene-1,1-dioxide), a small–molecule inhibitor of signal transducer and activator of transcription 3 (STAT3), inhibited both ICAM–1 and VCAM–1 expression stimulated with LPS. LPS induced IkappaBα (IκBα) degradation within 1 hour. Quercetin did not affect the IκBα degradation stimulated with LPS. However, in luciferase reporter assay, quercetin decreased the NF–kB activity. On the other hand, quercetin prevented LPS–mediated increase of STAT3 phosphorylation. Quercetin reduced LPS–mediated THP–1 monocyte adhesion to HUVEC, in a concentration–dependent manner. These data provide a novel mechanism where quercetin inhibits NF–kB and STAT3 activity resulting in suppression of ICAM–1 and VCAM–1 expressions in the vascular wall.