【Objective】To investigate the effects and mechanisms of Nrf2-ARE（nuclear factor erythroid-2 related factor-anti? oxidant response element）pathway on uremic serum-mediated endothelial dysfunction in human aortic endothelial cells.【Methods】 Human aortic endothelial cells were incubated in endothelial cell medium containing 10% normal serum，10% non-diabetic uremic serum or 10% diabetic uremic serum respectively，and 20 μmol/L tertiary butyl hydroquinone（tBHQ）were pretreated with cells to active Nrf2-ARE pathway. The cells apoptosis rate were measured by flow cytometry，and the synthesis of NO was detected by flow cytometry and immune fluorescent confocal，while the expression of P-eNOS Ser1177 /eNOS，and quinone oxidoreductase-1（NQO1） were measured by western blotting. The levels of malondialdehyde，superoxide dismutase，catalase，and glutathione in these cells were also measured with kits.【Results】Aortic endothelial cells incubated with uremic serum had a higher level of apoptosis rate and MDA （P < 0.05），and a lower level of NO systhesis，P-eNOS Ser1177 /eNOS expression，CAT，SOD，GSH（P < 0.05）. Pretreated with tBHQ can reduce the apoptosis rate and MDA level（P < 0.05），improve the amount of NO systhesis，the expression of P-eNOS Ser1177 /eNOS，the levels of CAT，SOD，and GSH in these cells（P < 0.05）.【Conclusion】Activation of Nrf2-ARE pathway can improve endothelial dysfunction in aortic endothelial cells induced by uremic serum，and its mechanism might be related with enhancement of the antioxi? dant stress.