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

本实验采用（1）脑缺血模型和（2）增强耐受的条件，研究了热休克蛋白72（HSP 72）在沙土鼠脑缺血耐受中的作用。还通过使用近红外光谱检查了获得缺血耐受下的氧代谢。对一侧大脑半球进行10分钟的中度缺血预处理是可逆的，但足以产生HSP 72。在缺血30分钟后，两天前给予的处理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美拉烷（Bifemelane hydrochloride）（Life Sci.59：979-985：1996）成功地诱导了耐受性的增强。然而，与单次缺血预处理相比，增强耐受后HSP 72的增加并不显著。用近红外光谱法对脑内氧合状态的研究表明，缺血预处理可诱导随后缺血期间氧代谢的改善（Stroke 28：1451-1457：1997）。提示：（1）局灶性脑缺血可引起缺血耐受;（2）HSP 72可能参与缺血耐受的形成，但HSP 72不是唯一的缺血耐受分子，也可能不是主要的缺血耐受分子;（3）氧代谢的改善可能与缺血耐受的获得有关。

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.