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目的 通过观察脑缺血再灌注后海马CA1区存活神经元数目、原位末端标记 (TUNEL)阳性细胞数目、热休克蛋白 70 (HSP70 )阳性细胞数目以及脑组织超微结构的变化 ,探讨山莨菪碱 (Anisodamine ,Ani)对脑缺血再灌注损伤保护作用的机制。方法 采用Pulsinelli法建立大鼠全脑缺血再灌注损伤模型。观察Ani在脑缺血再灌注的迟发性损伤阶段对海马CA1区存活神经元数目、TUNEL阳性细胞数目、HSP70阳性细胞数目以及脑组织超微结构的影响。结果 Ani可增加脑缺血再灌注后HSP70的表达 ,减少神经元凋亡的发生 ,提高神经元的存活数目。结论 Ani可减少脑缺血再灌注神经元凋亡 ,提高神经元的存活数目 ,对脑缺血再灌注损伤起保护作用。
Objective To investigate the changes of the number of neurons in hippocampal CA1 area, the number of TUNEL positive cells, the number of heat shock protein 70 (HSP70) positive cells and the ultrastructure of brain tissue after cerebral ischemia-reperfusion in rats Protective mechanism of Anisodamine on cerebral ischemia-reperfusion injury in rats. Methods Pulsinelli method was used to establish a rat model of global cerebral ischemia-reperfusion injury. To observe the effect of Ani on the number of neurons in hippocampal CA1 area, the number of TUNEL-positive cells, the number of HSP70-positive cells and the ultrastructure of brain tissue during the delayed injury of cerebral ischemia-reperfusion. Results Ani can increase the expression of HSP70 after cerebral ischemia-reperfusion, reduce the occurrence of neuronal apoptosis and increase the number of neurons. Conclusion Ani can reduce neuronal apoptosis after cerebral ischemia-reperfusion, increase the number of neurons and protect the cerebral ischemia-reperfusion injury.