Objective：To observe the effects of different levels of reactive oxygen species（ROS） and oxidative stress on cell proliferation，apoptosis，cycle in the renal tubular epithelial model of sepsis，and to explore whether oxidative stress and mitochondrial-Caspase pathway can be used as the therapeutic target of sepsis renal tubular epithelial injury. Methods：Human renal tubular epithelial HK-2 cells were treated with lipopolysaccharide（LPS） at a final concentration of 10 μg/mL for 12 h to establish a sepsis cell model. The sepsis cell model was randomly divided into H2O2 group（H2O2，300 μmol/L），Caspase inhibitor group（Ac-DEVD-CHO，15 μmol/L），Caspase inhibitor+H2O2 group（H2O2，300 μmol/L+Ac-DEVD-CHO，15 μmol/L） and negative control group（no treatment）. Normal cultured HK-2 cells were taken as the blank control group. the expression of Cleaved-Caspase-3 and Cleaved-poly ADP-ribose polymerase（PARP） protein were detected by Western blot， cell proliferation was detected by MTT，cell ROS levels，apoptosis and cell cycle were detected by flow cytometr. Results：The ROS， apoptosis rate，Cleaved-Caspase 3 and Cleaved-PARP level，the proportion of G1 cells in negative control group were all higher than those in blank control group（all P <0.05），the proliferation rate was lower than that of blank control group（P < 0.05）. The ROS，apoptosis rate，Cleaved-Caspase 3 and Cleaved-PARP level， the proportion of G1 cells in H2O2 group were all higher than those of negative control group（all P <0.05），the proliferation rate was lower than that of negative control group（P <0.05）. The ROS，apoptosis rate，Cleaved-Caspase 3 and Cleaved-PARP levels，the proportion of G1 cells in Caspase inhibitor+H2O2 group were all lower than those of H2O2 group（all P < 0.05），but were all higher than negative control group（P < 0.05），the proliferation rate was higher than that of H2O2 group（P < 0.05），but still lower than that of negative control group（P < 0.05）. Conclusion：The oxidative stress level of sepsis cell model is abnormally upregulated. Excessive ROS can inhibit the proliferation of septic renal tubular epithelial cells， promote cell apoptosis and cause cell cycle G1 block through the mitochondrial-Caspase pathway. Inhibition of Caspase has a certain protective effect on renal tubular epithelial cell injury in sepsis caused by ROS.