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摘要Objective Advanced glycation end products(AGEs) and endothelial progenitor cells(EPCs) play key roles in pathogenesis of diabetes-related vascular complications.AGEs can induce EPCs dysfunction.The peroxisome proliferator-activated receptor-gamma(PPARγ) agonists are widely used in the treatment of type 2 diabetes and it remains unknown if they could attenuate AGEs induced EPCs dysfunction.Methods EPCs isolated from healthy adults were cultured with various concentrations of AGEs(0,50,100 and 200 mg/L) in the absence and presence of rosiglitazone(10 nmol/L),anti-RAGE(receptor for AGEs)-HSA(human serum albumin) antibody(50 μg/ml),PI3k(phosphatidylinositol-3-kinase) inhibitor(LY294002,5 μmoL/L),nitric oxide inhibitor(L-NAME,100 μmol/L) or sodium nitroprusside (SNP,25 μmol/L).Prolfferation,apoptosis,cell adhesion,migration,and nitric oxide(NO) production of EPCs were assessed and expressions of eNOS and Akt were determined.Results Number,proliferation/migration capacities,eNOS and Akt phosphorylation as well as bioavailable NO of EPCs were increased by rosiglitazone and reduced by AGEs.AGEs also promoted while rosiglitazone reduced EPCs apoptosis.The AGEs induced effects could be significantly ameliorated by preincubation with rosiglitazone,RAGE antibody and SNP.The beneficial effect of rosiglitazone could be blocked by pretreatment with L-NAME and LY294002.Conclusion PPARγ agonist rosiglitazone could increase EPCs function and attenuate AGEs induced EPCs dysfunction via upregulating Akt-eNOS signal pathways of EPCs.