沙鼠脑缺血耐受的组织学变化及HSP在其中的作用

目的 :观察脑缺血耐受时的组织学变化及 HSP在其中的作用。方法 :通过 HE染色观察脑缺血耐受时的组织学变化 ,并通过免疫组化染色 ,了解 HSP70及 HSP2 7在其中的作用。结果 :一次性 5分钟缺血后 7天海马 CA1区神经元大多坏死 ,若在缺血前给予 2分钟的缺血预处理 ,该区神经元大多保留 ,表现出明显的保护作用。只给一次性 5分钟缺血 ,海马 CA1区神经元无 HSP70染色。若在缺血前给予预处理 ,海马 CA1区神经元可见明显 HSP70染色。而HSP2 7主要在胶质细胞表达 ,海马区的神经元未见其表达。结论 :缺血前给予预处理对以后的缺血有保护作用 ;在缺血耐受过程中 ,HSP70表达出一定的保护作用。

Histological findings and HSP analysis of ischemic tolerance in gerbil

Objective To investigated the histological findings and role of HSP in ischemic tolerance. Methods We investigated the histological findings with HE staining and the role of HSP with immunohistochemical analysis. Result Single 5 min ischemia consistantly caused neuronal loss in the hippocampal CA1 after 7 days recirculation. On the other hand, in double ischemic groups, 2 min ischemic insult 2 days before 5 min ischemia exhibited significant protection in hippocampus CA1. In the immunohistochemical analysis, 5 min ischemia without preconditioning caused no induction of HSP70 in CA1 of hippocampus. While 5 min ischemia with pretreatment, caused increased synthesis of HSP70 in the hippocampus, especially in CA1 of hippocampus. HSP27 was not stained in neuron in the hippocampus, which inducted in the glial cells in the hippocampus, mainly in the CA3 subfield and dentate hilus. Conclusion The preconditioning exhibited protection against neuronal death following subsequent ischemia. The synthesis of HSP70 is correlated with the protection, While HSP27 is unlikely to have a direct role in the mechanism of ischemic tolerance.