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目的:探讨预吸氧对新生鼠宫内脑再灌注损伤Caspase-3和iNOS的影响。方法:取孕21天Wistar大鼠制成脑缺血再灌注损伤模型。另有同日龄孕鼠分别在30%、50%和90%氧浓度下预吸氧30 min后,完成宫内缺血后再灌注模型的制备。取出新生鼠脑组织应用免疫组织化学分析检测Caspase-3和iNOS的阳性细胞数,同时应用病理组织学观察脑组织病理变化。结果:各组间Caspase-3和iNOS的阳性细胞数量差异有统计学意义。再灌注组和90%预吸氧组Caspase-3和iNOS的阳性细胞数量比对照组有明显增加。50%预吸氧组Caspase-3和iNOS的阳性细胞数量比再灌注1h组降低。30%和50%预吸氧组均可见以上神经元损伤改变,与缺血再灌注后无明显差别,而90%预吸氧组新生鼠脑组织病理改变加重,可见个别神经元细胞变性、凋亡。结论:再灌注损伤后,Caspase-3和iNOS的表达增加是脑损伤神经细胞凋亡的重要因素。高浓度预吸氧加重脑缺血再灌注损伤神经细胞凋亡,而50%预吸氧可能改善脑缺血再灌注损伤神经细胞凋亡。
Objective: To investigate the effect of preoxygenation on the expression of Caspase-3 and iNOS after intrauterine reperfusion injury in neonatal rats. Methods: Wistar rats were made into a model of cerebral ischemia-reperfusion injury on day 21 of pregnancy. Another pregnant mice of the same age were pre-oxygenated for 30 min at 30%, 50% and 90% oxygen concentration respectively to complete the intrauterine ischemia / reperfusion model preparation. Immunohistochemistry was used to detect the number of positive cells of Caspase-3 and iNOS in brain tissue of newborn rats. At the same time, pathological changes of brain tissues were observed by histopathology. Results: There was significant difference in the number of positive cells between Caspase-3 and iNOS in each group. Compared with the control group, the number of positive cells of Caspase-3 and iNOS in reperfusion group and 90% pre-oxygen group increased significantly. The number of positive cells of Caspase-3 and iNOS in 50% pre-oxygen group was lower than that in reperfusion group 1h. 30% and 50% pre-oxygenated group can be seen above the neuronal damage changes, with no significant difference after ischemia-reperfusion, and 90% pre-oxygen group neonatal rat brain tissue pathological changes increased, showing that some neuronal degeneration, apoptosis Death. Conclusion: The increased expression of Caspase-3 and iNOS after reperfusion injury is an important factor in the neuronal apoptosis of brain injury. High concentration of preoxygenation increased neuronal apoptosis after cerebral ischemia reperfusion injury, while 50% preoxygenation may improve neuronal apoptosis after cerebral ischemia-reperfusion injury.