Objective. To explore the regulation of endogenous sulfur dioxide on oxidative stress in lung injury induced by sepsis. Method. Forty male Sprague Dawley rats were divided into control, sepsis, sepsis + SO2, and SO2 group randomly used to observe survival rate. The other group of twenty-eight rats were randomly divided as the same manner for mechanism research. The number of WBCS and the percentage of PMN cells were calculated. The microphotographs of morphological changes and the index of quantitative assessment (IQA) of lung tissues were calculated. The ratio of wet/dry (W/D) of lung tissues was calculated. Levels of H2O2, MDA, NO, MPO, SOD, GSH-px, and TNF-α in plasma and lung tissues were measured. Result. The number of WBCS and the percentage of PMN cells decreased in sepsis ( p all < 0.05), and rebound in sepsis+SO2 ( p all < 0.05). The IQA and W/D of lung tissues increased in sepsis ( p for W / D < 0.05 ), and decreased in sepsis+SO2 ( p all < 0.05). H2O2 and MDA of plasma and lung tissues increased in sepsis ( p all < 0.05) and rebound in sepsis+SO2 ( p for H2O2 of plasma and lung tissues <0.05). NO and MPO of plasma and lung tissues increased in sepsis ( p for NO and MPO of lung tissues <0.05) and rebound in sepsis+SO2 ( p   all < 0.05 ). SOD of plasma and lung tissues in sepsis group decreased ( p all <0.05) and increased in sepsis+SO2 ( p all < 0.05). GSH-px of plasma and lung tissues decreased in sepsis ( p for plasma <0.05) and increased in sepsis+SO2 ( p for GSH-px of lung tissues <0.05). TNF-α of plasma and lung tissues increased in sepsis ( p all<0.05) and decreased in sepsis+SO2 ( p for lung tissue <0.05). Conclusion. Endogenous sulfur dioxide improves the survival rate of sepsis by improving the oxidative stress response during lung injury.