Department of Emergency Medicine, Beijing Jishuitan Hospital, Beijing 100035, China.
Department of Cardiology, Beijing Jishuitan Hospital, Beijing 100035, China.
Oxid Med Cell Longev. 2022 Feb 27;2022:6339355. doi: 10.1155/2022/6339355. eCollection 2022.
To explore the regulation of endogenous sulfur dioxide on oxidative stress in lung injury induced by sepsis.
Forty male Sprague Dawley rats were divided into control, sepsis, sepsis + SO, and SO 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 HO, MDA, NO, MPO, SOD, GSH-px, and TNF- in plasma and lung tissues were measured.
The number of WBCS and the percentage of PMN cells decreased in sepsis ( all < 0.05), and rebound in sepsis+SO ( all < 0.05). The IQA and W/D of lung tissues increased in sepsis ( for / < 0.05), and decreased in sepsis+SO ( all < 0.05). HO and MDA of plasma and lung tissues increased in sepsis ( all < 0.05) and rebound in sepsis+SO ( for HO of plasma and lung tissues <0.05). NO and MPO of plasma and lung tissues increased in sepsis ( for NO and MPO of lung tissues <0.05) and rebound in sepsis+SO ( all < 0.05). SOD of plasma and lung tissues in sepsis group decreased ( all <0.05) and increased in sepsis+SO ( all < 0.05). GSH-px of plasma and lung tissues decreased in sepsis ( for plasma <0.05) and increased in sepsis+SO ( for GSH-px of lung tissues <0.05). TNF- of plasma and lung tissues increased in sepsis ( all<0.05) and decreased in sepsis+SO ( for lung tissue <0.05).
Endogenous sulfur dioxide improves the survival rate of sepsis by improving the oxidative stress response during lung injury.
探讨内源性二氧化硫对脓毒症肺损伤氧化应激的调节作用。
40 只雄性 Sprague Dawley 大鼠随机分为对照组、脓毒症组、脓毒症+SO 组和 SO 组，观察生存率。另外 28 只大鼠随机分为同样的机制研究组。计算白细胞总数（WBCS）和中性粒细胞百分比（PMN）。计算肺组织形态变化的显微照片和定量评估指数（IQA）。计算肺组织的湿/干（W/D）比值。测量血浆和肺组织中 HO、MDA、NO、MPO、SOD、GSH-px 和 TNF-的水平。
脓毒症组 WBCS 数和 PMN 细胞百分比下降（均<0.05），脓毒症+SO 组反弹（均<0.05）。肺组织 IQA 和 W/D 增加（均<0.05），脓毒症+SO 组降低（均<0.05）。HO 和 MDA 增加（均<0.05），脓毒症+SO 组反弹（血浆和肺组织 HO 均<0.05）。NO 和 MPO 增加（肺组织 NO 和 MPO 均<0.05），脓毒症+SO 组反弹（均<0.05）。SOD 降低（均<0.05），脓毒症+SO 组增加（均<0.05）。GSH-px 降低（血浆均<0.05），脓毒症+SO 组增加（肺组织 GSH-px 均<0.05）。TNF-增加（均<0.05），脓毒症+SO 组降低（肺组织均<0.05）。
内源性二氧化硫通过改善脓毒症肺损伤时的氧化应激反应，提高脓毒症的生存率。
