论文部分内容阅读
目的:探讨围产期缺血缺氧对新生大鼠肺超微结构和肿瘤坏死因子α(TNFα-)及核因子κB抑制蛋白(κI-Bα)表达的影响。方法:结扎孕鼠一侧子宫角血管(另一侧宫内胎鼠作为对照),建立围产期缺血缺氧动物模型。电镜下观察肺组织超微结构变化并分别采用ELISA、RT-PCR和W estern b lot杂交法观察不同程度缺血缺氧新生大鼠肺组织TNFα-蛋白和mRNA及I-κBα表达的变化。结果:宫内急性缺血缺氧20 m in时,新生大鼠Ⅱ型肺泡上皮细胞和毛细血管内皮细胞受损;肺组织TNFα-蛋白和mRNA表达明显增强(P均<0.01),κI-Bα表达明显减弱(P<0.05),并随缺血缺氧时间延长病变加重。结论:围产期急性缺血缺氧致新生大鼠肺损伤,Iκ-Bα和TNFα-的异常表达可能是肺损伤的重要原因。
Objective: To investigate the effects of perinatal hypoxia on lung ultrastructure and expression of tumor necrosis factor-α (TNFα) and nuclear factor κB inhibitor (κB) in neonatal rats. Methods: Ligating the uterine horn blood vessels on one side of the pregnant rats (the other side of the uterus fetus as a control), establishment of animal model of perinatal hypoxia. The ultrastructural changes of lung tissue were observed under electron microscope. The changes of TNFα-protein and mRNA and I-κBα expression in lung tissue of hypoxic-ischemic rats were observed by ELISA, RT-PCR and Western blot respectively. Results: Type Ⅱ alveolar epithelial cells and capillary endothelial cells were impaired in neonatal rats with acute hypoxia and hypoxia for 20 minutes. The expression of TNFα-protein and mRNA in lung tissues were significantly increased (P <0.01) The expression was significantly decreased (P <0.05), and with the prolonged ischemia and hypoxia lesions increased. Conclusion: Abnormal expression of Iκ-Bα and TNFα-induced lung injury in neonatal rats during perinatal acute hypoxia may be an important cause of lung injury.