TEMPORAL PROFILE OF HEAT-SHOCK PROTEIN-70 SYNTHESIS IN ISCHEMIC TOLERANCE INDUCED BY PRECONDITIONING ISCHEMIA IN RAT HIPPOCAMPUS
TEMPORAL PROFILE OF HEAT-SHOCK PROTEIN-70 SYNTHESIS IN ISCHEMIC TOLERANCE INDUCED BY PRECONDITIONING ISCHEMIA IN RAT HIPPOCAMPUS
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DOI：
10.1016/0306-4522(93)90138-6
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发表时间：
1993-10-01
期刊：
影响因子：
3.3
通讯作者：
KOGURE, K
中科院分区：
文献类型：
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作者：
LIU, Y;KATO, H;KOGURE, K
本研究采用免疫组织化学方法研究了大鼠海马热休克蛋白70诱导表达的时间分布，以阐明亚致死量缺血预处理后缺血耐受的机制。虽然6分钟的前脑缺血产生严重的神经元损伤的海马CA1区，预处理3分钟的缺血，再灌注3天保护对CA1神经元损伤后6分钟的缺血。对热休克蛋白70的免疫组织化学染色表明，该蛋白质诱导在CA 1锥体细胞缺血3分钟后的1，3和7天，免疫染色是最强烈的3天后。热休克蛋白的合成观察CA 1，CA 3和齿状门神经元缺血6分钟后，1和3天，无论有和没有预处理。另外，预处理缺血6min后2h和7d，海马CA1区可见热休克蛋白染色，但染色强度较弱，提示亚致死性缺血诱导的应激反应对缺血性神经元损伤具有保护作用，包括在第二次缺血发作期间和之后立即合成热休克蛋白70，与保护相关，因为热休克蛋白的晚期诱导不能防止神经元死亡。
We investigated the temporal profile of heat shock protein 70 induction in the rat hippocampus using immunohistochemistry to clarify the mechanism of ischemic tolerance following preconditioning with sublethal ischemia. Although a 6-min period of forebrain ischemia produced severe neuronal damage to the hippocampal CA1 subfield, preconditioning with 3 min of ischemia followed by three days of reperfusion protected against the CA1 neuronal damage after 6 min of ischemia. Immunohistochemical staining against heat shock protein 70 showed that the protein is induced in CA1 pyramidal cells one, three and seven days after 3 min of ischemia, the immunostaining being most intense after three days. Heat shock protein synthesis was observed in CA1, CA3 and dentate hilar neurons one and three days after 6 min of ischemia, both with and without preconditioning. In addition, the heat shock protein was stained in the CA1 2 h and seven days after 6 min of ischemia with preconditioning, but the intensity of staining was relatively weak at these time points.The results suggest that stress response induced by sublethal ischemia protects against ischemic neuronal damage, and that the induced stress response, including heat shock protein 70 synthesis during and immediately after the second ischemic episode, is correlated with the protection because late induction of the heat shock protein did not prevent neuronal death.