Aim To investigate the effects of advanced glycation endproducts(AGE) on oxidative stress in bone-marrow derived endothelial progenitor cells(EPC) and the relationship of EPC functions. Methods Mononuclear cells(MNC) were isolated from rat bone marrow by Ficoll density gradient centrifugation and cultured for 7 days,EPC were identified as adherent cells double positive stained for FITC-UEA-Ⅰand DiI-acLDL under laser confocal immunofluence microscope.EPC were cultured in the absence or presence of AGE(50,100 and 200 mg/L).Reactivated oxygen species(ROS) were analyzed using the ROS assay kit.A spectrophotometer was used to assess superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) expression,and the PCR was also used to determine the mRNA expression.A modified Boyden's chamber was used to assess the migration of EPC and the number of recultured EPC was counted to measure the adhesiveness function.A spectrophotometer was used to determine the proliferation function. Results Co-culturing with AGE increased ROS production,decreased antioxidase and induced the proliferation,migration and adhesion of EPC inhibition in a dose dependent manner. Conclusion AGE increase oxidative stress and mediate impairment of progenitor cell function in a dose dependent manner,which indicates a new pathophysiological mechanism of disturbed vascular adaptation in atherosclerosis and suggests that lower levels of AGE might improve the success of progenitor cell therapy.