Simon R P, Niiro M, Gwinn R
Department of Neurology, University of California, San Francisco Medical Center 94143-0870.
Neurosci Lett. 1993 Dec 12;163(2):135-7. doi: 10.1016/0304-3940(93)90364-q.
We studied the possible role of prior ischemic stress as a protective mechanism against cerebral infarction in rats. Two brief periods of global cerebral ischemia, separated by 24 h, did not cause cell death in brain, but did produce neuronal stress, as demonstrated by induction of the nonconstitutive 72 kDa heat shock protein (HSP72). Forty-eight hours later, animals subjected to prior ischemia had smaller infarct from permanent middle cerebral artery occlusion than did sham-operated controls. These findings support an association between ischemia-induced stress, HSP72 induction, and attenuation of injury from subsequent focal cerebral ischemia.
我们研究了既往缺血应激作为大鼠脑梗死保护机制的潜在作用。两次短暂的全脑缺血,间隔24小时,并未导致脑内细胞死亡,但确实产生了神经元应激,这通过非组成型72 kDa热休克蛋白(HSP72)的诱导得以证明。48小时后,经历过既往缺血的动物在永久性大脑中动脉闭塞后形成的梗死灶比假手术对照组更小。这些发现支持了缺血诱导的应激、HSP72的诱导与随后局灶性脑缺血损伤减轻之间的关联。