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目的 探讨氧化/抗氧化及细胞因子在新生大鼠急性肺损伤中的变化。方法 用脂多糖(LPS)制备新生大鼠急性损伤模型,用化学方法和酶联免疫吸附法(ELISA)分别检测肺组织丙二醛(MDA)、超氧化物歧化酶(SOD)、白细胞介素-10(IL-10)和白细胞介素-18(IL-18)的改变。结果 MDA在应用LPS后1小时明显高于正常对照组,(31.99±1.73)nmol/mg肺蛋白VS(10.68±0.67)nmol/mg肺蛋白,持续至24小时;SOD含量在应用LPS后1小时即明显低于正常对照组,(69.86±2.94)NU/mg肺蛋白VS(85.99±1.89)NU/mg肺蛋白,4小时最低(58.61±3.01)NU/mg肺蛋白,8小时有所恢复,16小时基本正常;IL-10在注射LPS后4小时明显升高[(9.46±0.53)pg/mg肺蛋白],持续至16小时仍高于正常对照组(8.57±0.38)pg/mg肺蛋白,24小时下降至正常;IL-18在应用LPS后1小时即明显增多(10.73±0.29)pg/mg肺蛋白,持续至24小时。结论 在LPS造成的新生大鼠急性肺损伤中,存在明显的氧化/抗氧化平衡失调,并有抑炎性和促炎症介质的失调,炎症介质释放的失调和氧化/抗氧化的失衡可能相互协同,加重肺损伤。
Objective To investigate the changes of oxidative / anti-oxidation and cytokines in acute lung injury of neonatal rats. Methods Acute injury models of neonatal rats were established by lipopolysaccharide (LPS). The levels of malondialdehyde (MDA), superoxide dismutase (SOD), interleukin -10 (IL-10) and interleukin-18 (IL-18) changes. Results The level of MDA in the LPS group was significantly higher than that in the control group at 1 hour after LPS administration (31.99 ± 1.73) nmol / mg LPS (10.68 ± 0.67) nmol / mg LPS for up to 24 hours. The SOD level was 1 hour after LPS administration (69.86 ± 2.94) NU / mg lung protein VS (85.99 ± 1.89) NU / mg pulmonary protein, the lowest 4 hours (58.61 ± 3.01) NU / mg pulmonary protein, restored to the level of 8 hours, (9.46 ± 0.53) pg / mg pulmonary protein at 4 hours after LPS injection, and remained higher than that of the control group (8.57 ± 0.38) pg / mg pulmonary protein for 16 hours , Decreased to normal at 24 hours; IL-18 increased significantly (10.73 ± 0.29) pg / mg pulmonary protein at 1 hour after the application of LPS for up to 24 hours. Conclusions There is a clear imbalance of oxidative / anti-oxidant balance in acute lung injury induced by LPS in neonatal rats, as well as inhibition of inflammatory and proinflammatory mediators, imbalance of inflammatory mediator release, and imbalance of oxidation / antioxidation , Aggravating lung injury.