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Involvement of heat shock protein 72 in aquisition and augmentation of ischemic tolerance in gerbil brains

热休克蛋白 72 参与沙鼠大脑缺血耐受性的获得和增强

基本信息

批准号：
08457189
负责人：
YANAGIHARA Takehiko
金额：
$ 4.03万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1997
项目状态：
已结题

项目摘要

Involvement of heat shock protein 72 (HSP72) in ischemic tolerance in gerbil brain was examined by using (1) hemispheric ischemia model and (2) conditions to enhance tolerance. Oxygen metabolism under acquisition of ischemic tolerance was also examined by using a near-infrared spectroscopy. A moderate degree of ischemic pretreatment for 10 min to one hemisphere was reversible but strong enough to produce HSP72. The treatment given two days earlier induced neuronal protection in the caudoputamen after ischemia for 30 min (Brain Res.716 : 39-46 : 1996). We then successfully induced augmentation of tolerance by repetitive ischemic pretreatment (Neuroscience 81 : 989-998 : 1997) and by administartion of a neuroprotective agent, bifemelane hydrochloride (Life Sci.59 : 979-985 : 1996). However, the increase in HSP72 after augmentation of tolerance was not significantey more in comparison with a single ischemic pretreatment. The study for intracerebral oxygenation states with a near-infrared spectroscopy showed that ischemic pretreatment could induce improvement of oxygen metabolism during subsequent ischemia (Stroke 28 : 1451-1457 : 1997). These data suggested that (1) ischemic tolerance could be observed in focal cerebral ischemia, (2) involvement of HSP72 in ischemic tolerance was likely present but HSP72 was not a sole molecule responsible for ischemic tolerance and might not be the primary molecule, and (3) improvement in oxygen metabolism might be related to acquisition of ischemic tolerance.

通过使用（1）半球缺血模型和（2）增强耐受性的条件来检查热休克蛋白72（HSP72）在沙鼠脑缺血耐受中的参与。还通过使用近红外光谱检查了获得缺血耐受性下的氧代谢。对一侧半球进行 10 分钟的中等程度的缺血预处理是可逆的，但强度足以产生 HSP72。两天前给予的治疗在缺血30分钟后诱导尾壳核中的神经元保护(Brain Res.716:39-46:1996)。然后，我们通过重复缺血预处理（Neuroscience 81：989-998：1997）和通过施用神经保护剂盐酸双非美烷（Life Sci.59：979-985：1996）成功诱导耐受性增强。然而，与单次缺血预处理相比，增强耐受后HSP72的增加并不显着。利用近红外光谱对脑内氧合状态进行的研究表明，缺血预处理可以改善随后的缺血期间的氧代谢（Stroke 28：1451-1457：1997）。这些数据表明（1）在局灶性脑缺血中可以观察到缺血耐受性，（2）可能存在HSP72参与缺血耐受性，但HSP72不是负责缺血耐受性的唯一分子，并且可能不是主要分子，（3）氧代谢的改善可能与缺血耐受性的获得有关。