缺血预处理对缺血再灌注后神经元长期保护效应的观察

目的 动态观察缺血预处理后脑缺血大鼠脑皮层和海马CA1区神经元凋亡数和神经元数，探讨缺血预处理能否提供长时期神经元保护作用。方法 四血管阻断法复制全脑缺血模型，动物随机分为非缺血对照组、预处理对照组、缺血预处理组和缺血组。采用TUNEL和尼氏染色法观察缺血后不同时相点皮层及海马CA1区神经元凋亡细胞数和神经元数。结果 全脑缺血可诱导皮层及海马CA1区神经元凋亡；缺血预处理明显减少缺血再灌注后的神经元凋亡。缺血组神经元在缺血后7天明显减少．12周时大量减少；缺血预处理后7天神经元未见明显减少，但12周时仍然大量减少，与缺血组相比无显著差异。结论 全脑缺血可能通过诱导缺血区神经元凋亡，导致缺血区神经元的大量丢失；缺血预处理可在短时间内提供一定程度的神经元保护作用，但不能完全阻止缺血后神经元的凋亡，可能仅仅是推迟了缺血后神经元凋亡发生的进程。

Effects of Ischemic-preconditioning on Long-term Protection of Neurons Following Global Cerebral Ischemia and Reperfusion

Objective To dynamically observe the effects of ischemic preconditioning on neuronal apoptosis and survival neurons following global ischemia in the cortex and hippocampal CA1 region of rat in order to investigate whether ischemic preconditioning has the long term neuroprotection.Methods Global cerebral ischemia was induced in rats by four vessel occlusion.All rats were divided randomly into sham(S)group,preconditioning(P)group,ischemia preconditioning(IP)group,and cerebral ischemia(I)group.Terminal deoxynucleotidyl transferase(TdT) mediated dUTP nick end labeling(TUNEL)and Nissle staining were used to detect the numbers of apoptosis and survival neuron in the cortex and hippocampal CA1 region.Results Global cerebral ischemia can induce apoptosis in cortex and hippocampal CA1 region;Cerebral ischemic preconditioning can significantly suppress the neuronal apoptosis induced by ischemia and reperfusion.The survival neurons of cortex and hippocampus in group I reduced markedly after 7 days of global ischemia,and there were few alive neurons after 12 weeks of ischemia.The survival neurons of cortex and hippocampus in group IP showed no significant change after 7 days of global ischemia,but lost notability after 12 weeks following ischemia.The numbers of survival neurons in group IP were no significant difference compared with that in group I after 12 weeks following ischemia.Conclusion Global cerebral ischemia can lead to the neurons losing significant by inducing neuronal apoptosis.Ischemic preconditioning only just delayed apoptosis which induced by ischemia,but can't provide substantial and long term neuroprotection.