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目的:探讨维生素E对脂多糖(lipopolysaccharide,LPS)诱导的急性肺损伤(acute lung injury,ALI)中氧化应激状态的影响。方法:以Wistar大鼠为研究对象,实验分成正常对照组、ALI组及维生素E预处理组。用LPS作用于大鼠6 h后检测各组大鼠肺组织中丙二醛(Malondialdehyde,MDA)的含量、乳酸脱氢酶(lactate dehydrogenase,LDH)及超氧化物歧化酶(superoxide dismutase,SOD)活性,并应用RT-PCR及ELISA法检测大鼠肺组织中TNF-α的水平。结果:ALI组与正常对照组比较SOD活性下降、LDH的活性增强、MDA的含量升高,且TNF-αmRNA及蛋白的表达增加(P﹤0.05);维生素E预处理组与ALI组比较SOD活性增强,LDH的活性减弱,MDA的含量降低,TNF-αmRNA及蛋白的表达降低(P﹤0.05)。结论:维生素E预处理可减轻LPS诱导的ALI大鼠肺组织的脂质过氧化损伤,减少炎症因子的表达,发挥一定的抗损伤效应。
Objective: To investigate the effect of vitamin E on oxidative stress in acute lung injury (ALI) induced by lipopolysaccharide (LPS). Methods: Wistar rats were divided into normal control group, ALI group and vitamin E pretreatment group. Malondialdehyde (MDA), lactate dehydrogenase (LDH) and superoxide dismutase (SOD) in the lungs of rats were detected by LPS for 6 h. Activity, and the level of TNF-α in rat lung tissue was detected by RT-PCR and ELISA. Results: Compared with the normal control group, the SOD activity decreased, the activity of LDH increased, the content of MDA increased and the expression of TNF-αmRNA and protein increased in ALI group (P <0.05). Compared with ALI group, SOD activity (P <0.05). The activity of LDH decreased, the content of MDA decreased and the expression of TNF-αmRNA and protein decreased (P <0.05). Conclusion: Vitamin E preconditioning can attenuate the lipid peroxidation injury induced by LPS in lungs of ALI rats, reduce the expression of inflammatory cytokines and exert certain anti-inflammatory effects.