Aim To investigate the expression of endoplasmic reticulum stress(ESR) marker C/EBP homologous protein-10 (CHOP-10) in the human aortic endothelial cells (HAEC) under the ischemia and hypoxia stress and to study the effects of atorvastatin on the process. Methods The cultured HAEC were divided into normal control group, ischemia/hypoxia model group, ischemia/hypoxia plus CHOP-10 shRNA group and ischemia/hypoxia plus atorvastatin treatment group (0.1 mol/L, 1.0 mol/L, 10.0 mol/L). After 24 hours, the expression of CHOP-10 was detected by RT-PCR and the protein levels of CHOP-10, caspase-3 and caspase-8 were measured by Western blot. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) in the supernatant of cell culture medium were measured by ELISA. The CCK-8 test was used to measure cell proliferation. Results As compared with that of the control group, the CHOP-10 expression increased significantly in HAEC under the ischemia and hypoxia stress(P<0.01), the IL-6 and TNF-α level in the supernatant of cell culture medium were significantly higher than those of the control group(P<0.01). And the cells apoptosis increased and proliferation activity decreased significantly under the ischemia and hypoxia stress(P<0.01). The expression of CHOP-10 can be inhibited by atorvastatin in a dose-dependent manner in HAEC under the ischemia and hypoxia stress(P<0.01). Knock down CHOP-10 expression or application of atorvastatin treatment can inhibit cell apoptosis and increase proliferation activity in the cells of the ischemia/hypoxia group(P<0.01). Conclusions These findings indicate that ischemia and hypoxia can induce ESR and inflammation in HAEC. CHOP-10 expression up-regulated by ESR can increase cell apoptosis and decrease proliferation activity. Down-regulated CHOP-10 expression or application of atorvastatin treatment can reduce ESR under the ischemia and hypoxia stress and have a protective effect on vascular endothelial cells.