Citation

Intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), P and Eselectin play a key role for the initiation of vascular inflammation. In this study, we explored the mechanism by which quercetin may inhibit ICAM1 and VCAM1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVEC). Quercetin prevented LPSmediated increase of ICAM1 and VCAM1 expression. Stattic (6- Nitrobenzo[b]thiophene-1,1-dioxide), a smallmolecule inhibitor of signal transducer and activator of transcription 3 (STAT3), inhibited both ICAM1 and VCAM1 expression stimulated with LPS. LPS induced IkappaB (IB) degradation within 1 hour. Quercetin did not affect the IB degradation stimulated with LPS. However, in luciferase reporter assay, quercetin decreased the NFkB activity. On the other hand, quercetin prevented LPSmediated increase of STAT3 phosphorylation. Quercetin reduced LPSmediated THP1 monocyte adhesion to HUVEC, in a concentrationdependent manner. These data provide a novel mechanism where quercetin inhibits NFkB and STAT3 activity resulting in suppression of ICAM1 and VCAM1 expressions in the vascular wall.