摘要
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
Objective The number of surviving neuron,TUNEL positive neurons,HSP70 expression and the ultrastructure of the CA 1 subfield of hippocampus were examined after cerebral ischemia/reperfusion in rats and the protective effects of L tetrahydropalmatine(L THP) were also observed.Methods Pulsinellis methods were employed to establish cerebral ischemia/reperfusion animal models.The abovementioned indices were examined with and without L THP.Results L THP could upregulate the expression of HSP70 after cerebral ischemia/reperfusion.Neuronal apoptosis after cerebral ischemia/reperfusion was decreased and the number of surviving neuron was increased by L THP.Conclusion L THP had remarkable protection on cerebral ischemia/reperfusion injury.Its mechanism might be related to decreasing neuronal apoptosis. [
出处
《中华急诊医学杂志》
CAS
CSCD
2001年第6期386-388,共3页
Chinese Journal of Emergency Medicine