Ischemic Neuronal Damade and heat Shock (Stress) Protein

我们研究了给予高温或轻度缺血处理的神经细胞获得对随后的致死性缺血应激的耐受性的可能性。将大鼠置于维持在42ﾟC的水浴中，产生高温。将大鼠的体温升高到42ﾟC 15分钟，然后进行四血管阻断15分钟。再循环7天后处死动物，取出脑组织，用10%福尔马林固定，苏木精-伊红染色进行组织病理学检查。在高温后8小时或24小时四支血管阻断15分钟的大鼠中，CA1区的缺血性神经元变化较未高温的四支血管阻断15分钟的小。用免疫印迹技术对高温动物的海马体进行分析。热休克蛋白70(HSP70)在高温后8小时和24小时均有表达，缺血8分钟后15分钟再缺血24小时对缺血性神经元改变有保护作用。热休克蛋白70在缺血8分钟后24小时即可在海马区表达，而在缺血15分钟后未见表达。这一结果支持了高温或轻度缺血使神经细胞对缺血损伤具有更强的抵抗力的可能性。提示这些对缺血应激的耐受性与HSP70的表达有关。

We investigated the possibility that neuronal cells given a hyperthermic or mild ischemia treatment acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo.Hyperthermia was produced in the rat by placing them in a water bath maintained at 42ﾟ C. The body temperature of the rat was raised to 42ﾟ C for 15 min and then the animals were subjected to 15 min of four-vessel occlusion. Seven days after recirculation, the animals were sacrificed, and the brains were removed, fixed in 10% formalin and stained by hematoxylin-eosin for histopathology. In the rat subjected to 15 min of four-vessel occlusion 8 or 24 hours after hyperthermia, ischemic neuronal change in the CA1 was less compared to 15 min of four-vessel occlusion without hyperthermia. The hippocampus from animals subjected to hyperthermia was analysed using immunoblotting. Expression of heat shock proteon 70(HSP 70)was shown in the animals 8 or 24 hours after hyperthermia.Eight min ischemia 24 hours before 15 min ischemia exhibited protective effect against ischemic neuronal change. Expression of HSP 70 was shown in the hippocampus 24 hours after 8 min ischemia, but was not after 15 min ischemia.These results provides support for the possibility that hyperthermia or mild ischemia makes the neuronal cells more resistant to the ischemic damage. It is suggested that these tolerance to the ischemic stress correlates to expression of HSP 70.