Abstract
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.
Highlights
Sepsis could be induced by severe trauma, injury, shock, and major surgery
The survival rates of rats in sepsis+ SO2 group were improved compared to the sepsis group at 12 h, 24 h, 36 h, 48 h, and 72 h after the operation, but the difference were not statistically significant (p = 1:000, 1.000, 0.371, 0.171, and 0.171, respectively, Figure 1, Table 1)
Sepsis is a common and critical complication, which could be induced by severe trauma, injury, shock, or major surgery
Summary
To explore the regulation of endogenous sulfur dioxide on oxidative stress in lung injury induced by sepsis. 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). 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
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