Resveratrol protects late endothelial progenitor cells from TNF--induced inflammatory damage by upregulating Kruppel-like factor-2

Cardiovascular risk factors can negatively influence late endothelial progenitor cell (EPCs) number and functions, thus EPCs biology is a clinical implications for cardiovascular diseases. The present study aimed to investigate the potential protective effects of resveratrol (RES) on tumor necrosis factor (TNF)--induced inflammatory damage in late endothelial progenitor cells (EPCs) and to elucidate the underlying mechanisms. Late EPCs at passages 3-5 were pretreated with RES at a concentration of 20 mu mol/l for 12 h and subsequently incubated with TNF- (10 ng/ml) for 24 h. The adhesion, migration, proliferation and vasculogenesis of EPCs were subsequently detected. Furthermore, the mRNA expression levels of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Nitric oxide (NO) levels in the supernatant were determined using a colorimetric assay kit. Additionally, the mRNA and protein expression of Kruppel-like factor-2 (KLF2) was determined by RT-qPCR and western blot analysis, respectively. The results indicated that TNF- markedly inhibited the proliferation, adhesion, migration and vasculogenesis of late EPCs. However, RES ameliorated the effects induced by TNF-. Furthermore, exposure of EPCs to TNF- decreased the levels of NO secretion and KLF2 expression at the mRNA and protein levels, but upregulated the levels of inflammatory factors, including ICAM-1 and MCP-1, compared with the control group. RES significantly inhibited TNF--induced inflammatory damage through upregulation of KLF2 expression and downregulation of the expression of ICAM-1 and MCP-1. In conclusion, RES may exert protective effects on the cardiovascular system, as demonstrated by the amelioration of TNF--induced inflammation in EPCs following RES treatment, and may therefore be used in the future for the prevention of cardiovascular disease.