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目的 观察老年大鼠全脑缺血再灌注后神经元凋亡的规律 ,并探讨氧化损伤的机制。方法 利用四血管结扎法 ,建立老年大鼠全脑缺血再灌注模型 ,分别于缺血再灌注后 6h、1、3、5、7d计数海马锥体神经元存活数 ,原位末端标记法计数凋亡神经元数 ,电镜观察超微结构变化 ,并测定脑组织丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)活性。结果 老年大鼠全脑缺血再灌注后海马CA1区神经元凋亡损伤在再灌注后第 3天损伤最重 ,存活神经元数显著减少 ,电镜显示有凋亡改变。脑组织SOD和GSH Px活性降低 ,MDA含量升高 ,再灌注后 3d最为明显。结论 全脑缺血再灌注神经元凋亡损伤与氧自由基水平升高 ,抗氧化酶活性降低有关。
Objective To observe the regularity of neuronal apoptosis after global cerebral ischemia and reperfusion in aged rats and to explore the mechanism of oxidative damage. Methods The model of global cerebral ischemia-reperfusion in aged rats was established by four-vessel ligation. The survival of pyramidal neurons in hippocampus were counted at 6h, 1,3,5,7d after ischemia-reperfusion, The number of apoptotic neurons and ultrastructure changes were observed by electron microscope. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH Px) in the brain tissue were determined. Results Apoptosis of hippocampal CA1 neurons in the aged rats was most severely damaged on the 3rd day after reperfusion, and the number of surviving neurons was significantly decreased. Electron microscopy showed apoptosis. The activity of SOD and GSH Px in brain tissue decreased and the content of MDA increased. The most obvious was 3d after reperfusion. Conclusion The neuronal apoptosis induced by global cerebral ischemia and reperfusion has the relationship with the increase of oxygen free radicals and the decrease of the antioxidant enzyme activity.