Aim To investigate the effects of advanced glycation end products(AGE) on the expression of monocyte chemoattractant protein-1(MCP-1) and vascular cell adhesion molecule-1(VCAM-1) in human umbilical vein endothelial cell(HUVEC)and the intervention effect of atorvastatin. Methods Collagenase was used to isolate the endothelial cell from human umbilical vein;HUVEC were identified by immunocellochemistry and morphology;RT-PCR was performed to detect MCP-1,VCAM-1 and recepter for AGE(RAGE) mRNA expression;Reactive oxygen species(ROS) detectionkit was used to examine the level of ROS in HUVEC and inversion fluoescence microscope was used to observe the ROS level. Results The cultured cells were oval or polygon and retained cobblestone appearance through inverted phase contrast microscope,brown particles could be observed in cytoplasm(CD31 or CD34 positive cells) after immunocytochemical staining with CD31 or CD34;In comparison with control group,AGE(10-4~10-1 g/L)promoted MCP-1 and VCAM-1 mRNA expression in a concentration-dependent manner in HUVEC.The expression of MCP-1 and VCAM-1 mRNA was significantly elevated by AGE(10-4 g/L) compared with the control group(0.26±0.02 vs 0.17±0.04;0.22±0.02 vs 0.08±0.01,P<0.01);Compared with AGE group,atorvastatin(0.1,1,10 μmol/L) diminished MCP-1 and VCAM-1 mRNA expression induced by AGE in HUVEC in a concentration-dependent manner;Atorvastatin in a dose of 1 μmol/L,could significantly decrease the expression of MCP-1 and VCAM-1 mRNA induced by AGE(0.63±0.11 vs 1.03±0.07;0.21±0.03 vs 0.83±0.10,P<0.01);The level of ROS in AGE group was higher than that in control group,atorvastatin could obviously decline the ROS level induced by AGE in HUVEC.Furthermore,atorvastatin(0.1 μmol/L) was able to decrease RAGE mRNA expression remarkly induced by AGE in HUVEC(0.63±0.05 vs 1.19±0.12,P<0.01). Conclusion AGE could significantly increase MCP-1 and VCAM-1 mRNA expression in HUVEC;Atorvastatin could decrease the oxidative stress and inflammation gene expression induced by AGE in HUVEC through inhibiting the expression of RAGE.