Resveratrol prevents TNF-α-induced VCAM-1 and ICAM-1 upregulation in endothelial progenitor cells via reduction of NF-κB activation

Objective To assess the effects of resveratrol (RSV) on expression of adhesion molecules in endothelial progenitor cells (EPCs) following tumor necrosis factor-alpha (TNF-alpha) stimulation. Methods EPCs were treated with RSV and stimulated with TNF-alpha. A mononuclear cell (MNC) adhesion assay was used to assess the effects of RSV on TNF-alpha-induced MNC adhesion. Vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin expression levels and nuclear factor kappa B (NF-kappa B) activation were assessed by immunoblotting. Results MNC adhesion to TNF-alpha-treated EPCs and VCAM-1/ICAM-1/E-selectin levels in EPCs were increased following TNF-alpha stimulation and decreased following RSV treatment. TNF-alpha enhanced NF-kappa B inhibitor alpha (I kappa B-alpha) phosphorylation in the cytosol as well as nuclear NF-kappa B p65 levels, both of which were decreased by RSV. Conclusions These findings provide new insights into RSV's anti-inflammatory and anti-atherosclerotic effects. RSV's mechanism of action might involve downregulation of VCAM-1, ICAM-1 and E-selectin by partial blockade of TNF-alpha-induced NF-kappa B activation and I kappa B-alpha phosphorylation in EPCs.