Aim To detect the effects of advanced glycation end products(AGE) on prostacyclin and prostaglandin E₂ expressions in culture endothelial cell and its possible mechanism. Methods ECV304 cell were exposed to 50,100,200,400 mg/L AGE or human serum albumin for 24 hours.The levels of 6-keto-prostaglandin F_(1α)(PGF_(1α)) and prostaglandin E₂(PGE₂) in the supernatants were measured by enzyme linked immunosorbent assay(ELISA).The expressions of cyclooxyenase-2(COX-2) mRNA and protein were detected by reverse transcription polymerase chain reaction(RT-PCR) and immunohistochemistric assay.The effects of receptor for AGE,nuclear factor-kappaB(NF-κB) single/double gene antisense RNA on the productions of 6-keto-PGF_(1α) and PGE₂ induced by AGE were measured by ELISA. Results The productions of 6-keto-PGF_(1α) and PGE₂ in the supernatants were higher in the cell treated by AGE,with a dose-dependent manner(p<0.01).The levels of COX-2 mRNA and protein were significantly higher in the cell treated by AGE(p<0.01).Receptor for AGE,NF-κB single/double gene antisense RNA could inhibit the productions of 6-keto-PGF_(1α) and PGE₂ treated by AGE(p<0.05 or 0.01).The inhibition of double gene antisense RNA were more effective than single gene antisense RNA(p<0.05). Conclusion AGE,via receptor for AGE,NF-κB signaling,induced upregulation of COX-2,resulting in induced prostacyclin and PGE₂ synthesis.This chain of events might contribute to the pathogenesis of inflammatory vascular injury.