To investigate the role of advanced glycation endproducts (AGEs) in the pathogenesis of age-related macular degeneration (AMD). ·METHODS: Bovine choroidal endothelial cells (CEC) were isolated by the modified protocol using lycopersicon esculentum agglutinin coated Dynabeads, and identified by immunocytochemical staining with anti-Factor VIII antibody and uptaking of dil-acetylated low-density lipoprotein (dil-ac-LDL). AGEs were prepared by incubating 50g/L bovine serum albumin and 150g/L glucose at 37益for 6 weeks, which were characterized by dot blot assay with anti- AGEs antibody. CEC proliferation was evaluated by 3, (4,5-dimethylthiazol-2-yl)-2,5- diphenyl tetrazolium bromide (MTT) assay, and tube formation in CEC was determined by a Vitrogen system. ·RESULTS: More than 90% of the cultured cells were positive to Factor VIII immunostaining and had the ability to uptake dil-ac-LDL, which were the features of endothelial cells. 219AGEs we prepared were affinitive to anti-AGEs antibody. After treatment with AGEs for a time course of 3 days, CEC proliferation was significantly increased in a dose-dependent manner by AGEs at concentrations between 62.5mg/L and 500mg/L. The cytokine, basic fibroblast growth factor (bFGF), enhanced strongly tube-like structure formation in CEC to 124%( <0.05) above that of untreated c ontrols. In this condition, AGEs at the concentrations of 500mg/L and 50mg/L showed no effect on CEC tube formation ( >0.05). ·CONCLUSION: The present study demonstrated that CEC proliferation was increased by AGEs. However, there was no statistical effect on CEC tube formation. These findings confirm and extend that AGEs could be a potential initiator in the pathogenesis of choroidal neovascularization in exudative AMD, at least in part, through enhancement of CEC proliferation