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目的 通过观察脑缺血再灌流后海马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 )的表达以及脑组织超微结构的变化 ,探讨左旋四氢巴马汀 (L THP)对脑缺血 再灌流损伤的保护作用的机制。方法 采用Pulsinelli法建立大鼠全脑缺血 再灌流损伤模型。观察L THP在脑缺血 再灌流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的表达以及脑组织超微结构的影响。结果 L THP可增加脑缺血 再灌流后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 L THP可减少脑缺血 再灌流神经元凋亡 ,提高神经元的存活数目 ,对脑缺血 再灌流损伤起保护作用
Objective To observe the number of neurons in hippocampal CA1 area, the number of TUNEL positive cells, the expression of heat shock protein 70 (HSP70) and the ultrastructure of brain tissue after cerebral ischemic reperfusion in rats. Mechanism of protective effect of palmatine (L THP) on cerebral ischemia-reperfusion injury. Methods Pulsinelli method was used to establish the rat model of global cerebral ischemia and reperfusion injury. To observe the effect of L THP on the number of neurons, the number of TUNEL positive cells, the expression of HSP70 and the ultrastructure of brain tissue in the hippocampal CA1 subregion in the period of delayed injury after cerebral ischemia-reperfusion. Results L THP can increase the expression of HSP70 after cerebral ischemia-reperfusion, reduce the occurrence of neuronal apoptosis and increase the number of neurons. Conclusion L THP can reduce the neuronal apoptosis in cerebral ischemia and reperfusion, increase the number of neurons and protect the cerebral ischemia-reperfusion injury