山莨菪碱在大鼠脑缺血再灌注时对神经元凋亡的影响  

Influence of Anisodamine on neuronal apoptosis after cerebral ischemia reperfusion in the rats

作　　者：蒋崇慧[1] 杨光田[1] 汤彦[1] 

机构地区：[1]同济医科大学附属同济医院急诊科,武汉430030

出　　处：《中国急救医学》2001年第3期131-133,共3页Chinese Journal of Critical Care Medicine

摘　　要：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 The number of surviving neuron,TUNEL positive neuron,HSP70 positive neuron and the ultrastructure of the CA1 subfield of hippocampus was detected after the cerebral ischemia reperfusion of rats and the protective effects of anisodamine(Ani) were also observed.Methods Pulsinelli’s method was employed to establish cerebral ischemia-reperfusion animal models.Observing the influence of Ani on the number of surviving neuron,TUNEL positive neuron,HSP70 positive neuron and ultrastructure of the CA1 subfield of hippocampus.Results Ani could induce upregulation of HSP70 expression after cerebral ischemia reperfusion.Neuronal apoptosis after cerebral ischemia reperfusion was decreased and the surviving number of pyramidal cells in hippocampus CA1 was increased by Ani. Conclusion Ani have a remarkable protection on cerebral ischemia reperfusion damage.Its mechanism may be related with decreasing the neuronal apoptosis.

关 键 词：脑缺血 再灌注损伤 热休克蛋白70 山莨菪碱 神经元调亡 大鼠 

分 类 号：R965[医药卫生—药理学]