INHIBITION OF NF–KB AND STAT3 BY QUERCETIN WITH
SUPPRESSION OF ADHESION MOLECULE EXPRESSION IN
VASCULAR ENDOTHELIAL CELLS
YOUNG-SUK CHO1#, CHAN HYUNG KIM1#, TAE–SUN HA2, HEE YUL AHN1*
1Department of Pharmacology, College of Medicine, Chungbuk University, Cheongju, 362-763 Republic of Korea
2Department of Pediatrics, College of Medicine, Chungbuk University, Cheongju, 362-763 Republic of Korea
*corresponding author: hyahn@chungbuk.ac.kr
#Authors have equal contribution
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Abstract:
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.

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