Aim To explore whether Cariporide exerts beneficial effect on impaired vascular endothelial function elicited by exogenous advanced oxidation protein products (AOPP), and to investigate the potential mechanisms. Methods Male SD rats were killed by exsanguination after anesthesia with pentobarbital sodium (30 mg/kg, IP). The thoracic aorta was immediately isolated and was cut into 3 ～ 4 mm rings. AOPP was prepared according to the methods of article. Rat aortic isolated rings were incubated with AOPP (1, 2, 3 mmol/L) and Cariporide (0.01～1 μmol/L) for 90 min. Endothelium-dependent relaxation (EDR) induced by acetylcholine (Ach), endothelium-independent relaxation induced by sodium nitroprusside (SNP), superoxide dismutase (SOD) activity, malondialdehyde (MDA) and nitric oxide (NO) were measured in rat isolated aorta. Results Co-incubation of aortic rings with AOPP-BSA (3 mmol/L) for 90 min resulted in a significant inhibition of EDR response to Ach. Cariporide (0.01～1 μmol/L) groups were significantly attenuated the inhibition of EDR response induced by AOPP-BSA. Conclusion Cariporide was able to protect against vascular endothelial dysfunction caused by AOPP-BSA. The mechanisms may be involved in antioxidative stress and increasing the synthesization and release of NO.