摘要
目的 探讨脑缺血预处理联合山莨菪碱 (Anisodamine,Ani)治疗对脑缺血再灌注损伤的保护作用及其机制。方法 采用大鼠全脑缺血再灌注损伤模型 ,观察脑缺血预处理及Ani在脑缺血再灌注时对海马CA1区HSP70蛋白的表达、存活神经元数目及脑组织超微结构的影响。结果 脑缺血预处理联合Ani治疗可使脑缺血再灌注时海马CA1区HSP70蛋白的表达快速而持久 ,并可减轻脑组织超微结构的损害 ,减少神经元的丢失 ,提高神经元的存活数目。结论 脑缺血预处理联合Ani治疗可增加脑缺血再灌注时HSP70蛋白的表达 ,提高存活神经元数目 。
Objective To investigate the protective effects and the mechanisms of cerebral ischemia preconditioning combined with Anisodamine (Ani) on cerebral ischemia-reperfusion injury of rats.Methods Pulsinelli's method was employed to establish acute cerebral ischemia-reperfusion animal models.Observing the influence of cerebral ischemia preconditioning combined with Ani on the expression of HSP70,the number of surviving neuron and ultrastructure of the CA1 subfield of hippocampus.Results The combined use of cerebral ischemia preconditioning and Ani could make the expression of HSP70 rapid and prolonged and the surviving number of pyramidal cells in hippocampus CA1 was increased.Conclusion Cerebral ischemia preconditioning combined with Ani could up-regulate the expression of HSP70,increase the survival neuron number and protect the cerebral ischemia-reperfusion injury.
出处
《中国急救医学》
CAS
CSCD
北大核心
2002年第1期26-28,共3页
Chinese Journal of Critical Care Medicine
关键词
脑缺血
再灌注损伤
热休克蛋白70
缺血预处理
山莨菪碱
大鼠
Cerebral ischemia-reperfusion
Heat shock protein 70
Cerebral ischemia preconditioning
Anisodamine
