Gobbel G T, Chan T Y, Chan P H
Department of Neurological Surgery, University of California, San Francisco 94143, USA.
Mol Chem Neuropathol. 1995 Feb-Apr;24(2-3):107-20. doi: 10.1007/BF02962137.
Induction of the 70 kDa heat shock protein (HSP70) by hypoxia and/or hypoglycemia and the effects of prior heat shock on injury owing to hypoxia and/or hypoglycemia were studied in rat cerebral endothelial cells. Hypoxia and/or hypoglycemia treatment resulted in increased expression of HSP70 only when such treatment was sufficient to cause detectable injury and when the initial treatment was followed by exposure of the cells to 24 h of normoxia and normoglycemia. Heat shock induced 24 h prior to treatment with 48 h of hypoxia slightly reduced endothelial cell damage as measured by fraction of lactate dehydrogenase release (10% decrease in injury). There was a more dramatic effect of prior heat shock on the moderate damage produced by 12 h of combined hypoxia and hypoglycemia (45% decrease), whereas the severe damage produced by 24 h of hypoxia and hypoglycemia was decreased by prior heat shock by only 16%. These results indicate that the hypoxia and hypoglycemia occurring in conjunction with ischemia are more likely to result in heat shock protein expression when there is injury to the tissue. Furthermore, heat shock protects cerebral endothelial cells from hypoxia and hypoglycemia either by slowing the initial development of injury or by delaying the onset of injury.
在大鼠脑内皮细胞中研究了缺氧和/或低血糖对70 kDa热休克蛋白（HSP70）的诱导作用，以及预先热休克对缺氧和/或低血糖所致损伤的影响。只有当缺氧和/或低血糖处理足以导致可检测到的损伤，且在初始处理后将细胞暴露于24小时的常氧和常糖环境时，该处理才会导致HSP70表达增加。在缺氧48小时处理前24小时进行热休克，通过乳酸脱氢酶释放分数测量，可轻微降低内皮细胞损伤（损伤减少10%）。预先热休克对12小时缺氧合并低血糖所致的中度损伤有更显著的影响（损伤减少45%），而24小时缺氧和低血糖所致的严重损伤经预先热休克后仅减少16%。这些结果表明，与缺血相关的缺氧和低血糖在组织受损时更有可能导致热休克蛋白表达。此外，热休克通过减缓损伤的初始发展或延迟损伤的发生来保护脑内皮细胞免受缺氧和低血糖的影响。
