大鼠局灶性脑梗死后细胞凋亡及热休克蛋白70表达的变化

目的 探讨大鼠局灶性脑梗死后热休克蛋白70(HSP70)及细胞凋亡的变化。方法采用光化学法诱导制作大鼠局灶性脑梗死模型，冰冻切片行HSP70免疫组化染色，并用TdT-介导duTP-生物缺口末端标记(TUNEL)法检测凋亡细胞。结果免疫组化显示对照组和假手术组动物无HSP70免疫反应；局灶性脑梗死组12h即有：HSP70的表达，48h时HSP70表达至高峰，阳性反应局限于半暗带。TUNEL结果显示，对照组和假手术动物无凋亡细胞；局灶性脑梗死组6h时在半暗区凋亡细胞出现，3d达高峰。结论局灶性脑梗死可诱导HSP70的表达、神经细胞凋亡，两者的分布一致，但HSP70的表达高峰明显早于细胞凋亡。

Dynamical Progression of the Temporal and Profile of HSP70 and Cell Apoptosis Following Focal Cerebral Infarction

Objective To observe the relation of heat shock protein 70(HSP70)and cell apoptosis in response to focal cerebral infarction.Methods To establish the model of focal cerebral infarction based on the principle of photochemical initiation of thrombosis.Brain sections at the level of striatum were for immunohistochemistry and DNA nick end-labeling(TUNEL).Results Immunohistochemical analysis revealed no HSP70-immunoreactivity in Group A and Group B rats.However,in Group C rats,HSP70 was expressed in penumbra at 12h.At 48h,HSP70 immunoreactivities were increased to the maximum in penumbra.TUNEL staining showed that there was no cell apoptosis in Group A or in Group B.However,in Group C,TUNEL-positive neurons were observed in the penumbra at 6h.At 48h,3 and 4days,the number was increased to the maximum in penumbra and there was more significant difference than other time points. Conclusion Focal cerebral infarction could induce the HSP70 expression and induce neurons apoptosis.The HSP70 expression and neuron apoptosis occurred in penumbra.The peak of HSP70 was earlier than cell apoptosis.