摘要
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 oxidation/antixidation and eytokines in lipopelysaccharide(LPS)-induced acute lung injury in neonatal rat. Methods LPS was used to make a neonatal rat model of acute lung injury. The levels of maleic dialdehyde(MDA), superoxide dismutase(SOD), interleukin-10(IL-10) and interleukin-18(IL-18) in lung tissue were detected, using chemical methods and Enzyme-Linded Immunosorbent Assay(ELISA). Results The level of MDA significantly ineredsed at 1 hour after LPS administration compared with normal control(31.99±1.73)nmol/mg lung protein VS(10.68±0.67)nmol/mg lung protein and this lasted 24 hours. SOD significantly decreased at 1 hour after LPS adminiatration, (69.86±2.96)NU/mg lung protein, and it was lowest at 4 hour, (58.61±3.01)NU/mg lung protein. IL-10 increased at 4 hour(9.46±0.53)pg/mg lung protein, lasting to 16 hour. IL-18 significantly increased at 1 hour, (10.73±0.29)pg/mg lung protein, maintaining higher level to 24 hour. Conclusion In LPS-induced acute lung injury of neonatal rat, the disturbance of oxidation antioxidation and inhibitory promotive cytokines play a role, and this may exacerbate acute lung injury.
出处
《新生儿科杂志》
2004年第2期69-72,94,共5页
The Journal of Neonatology
