Resveratrol prevents endothelial progenitor cells from senescence and reduces the oxidative reaction via PPAR-γ/HO-1 pathways

Figure 1.. Effect of RSV on the oxidative reaction of endothelial progenitor cells. (A) RSV decreased DCF fluorescence in a concentration-dependent manner. Representative flow cytometry results indicated that with the increase of the concentration of RSV, ROS production gradually reduced. (B) Pretreatment with RSV significantly reduced the NADPH oxidative activity in a concentration-dependent manner. (C) Stimulation with RSV led to a concentration-dependent increase of NO production. *P<0.05, **P<0.01, ***P<0.001 vs. the control. RSV, resveratrol; ROS, reactive oxygen species; NO, nitric oxide.

Figure 2.. Effect of RSV inhibiting premature senescence in EPCs with the increased expression of h-TERT and suppression of SIRT1 expression. (A) Representative photomicrographs demonstrated senescence-associated β-galactosidase positive cells (blue) in EPCs treated with RSV. Magnification, ×40. (B) Data is presented as mean ± standard error of the mean. (C) RSV increased the h-TERT protein expression levels in a dose-dependent manner, and the expression of SIRT1 was reduced. **P<0.01 vs. the control. EPC, endothelial progenitor cells; h-TERT, human telomerase reverse transcriptase; SIRT1, sirtuin 1.

Figure 3.. Effects of RSV on the PPAR-γ/HO-1 signaling pathway. Treatment with RSV increased (A) PPAR-γ and (B) HO-1 protein expression levels in a dose-dependent manner. **P<0.01 vs. the control. PPAR-γ, peroxisome proliferator-activated receptor-γ; HO-1, heme oxygenase-1; RVS, resveratrol.

Figure 4.. Effect of RSV on the recruitment of EPCs. The EPCs repaired the injured artery. However, the high concentration of RSV enhanced the re-endothelialization capacity of EPCs. Data were presented as the mean ± standard error of the mean. **P<0.01 vs. the control, #P<0.05 vs. the EPCs transplantation. EPC, endothelial progenitor cell; RSV, resveratrol.