老年大鼠全脑缺血再灌注所致神经元凋亡及氧化损伤的机制

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。

The mechanism of oxygen stress and neuron apoptosis during complete cerebral ischemia-reperfusion injury in aging rats

Objective To investigate the mechanism of neuron apoptosis and the regularity of oxygen stress during complete cerebral ischemia-reperfusion injury in aging rats.Methods Complete cerebral ischemia-reperfusion injury models were created by using four-vessel ligation.The rat's brain was removed after 6 h,1 d,2 d,3 d,5 d and 7 d of ischemia-reperfusion.The numbers of survival and apoptotic neurons which were stained by HE and TUNEL were counted in hippocampal CA1.The ultrastructure was also observed.The malondialdehyde(MDA),superoxide dismutase (SOD),glutathione peroxidase (GSH-PX) were assayed.Results The number of survival neurons increased remarkably,while apoptotic neurons were reduced.Electron microscopy also indicated apoptotic changes.The neurons were injured most severely 3 d after ischemia-reperfusion.The MDA contents inreased significantly,SOD and GSH-PX activity decreased,especially 3 d after ischemia-reperfusion.Conclusion The apoptotic mechanism during complete cerebral ischemia-reperfusion was related to increase in oxygen free radicals and decrease in antioxidase activity.