Araki T, Kato H, Liu X H, Kogure K, Itoyama Y
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Metab Brain Dis. 1994 Dec;9(4):369-75. doi: 10.1007/BF02098883.
Immunohistochemical changes of heat shock protein 70 (HSP 70) and glial fibrillary acidic protein (GFAP) were investigated in the gerbil hippocampus 1 h-7 days after 10 min of cerebral ischemia. Transient cerebral ischemia caused HSP 70 expression in GFAP-positive astrocytes in a delayed fashion, as compared with a rapid induction in vulnerable neurons such as hilar neurons. The present results may offer clues to elucidate the mechanisms of ischemic neuronal damage.
在沙土鼠大脑缺血10分钟后1小时至7天期间，研究了热休克蛋白70（HSP 70）和胶质纤维酸性蛋白（GFAP）的免疫组化变化。与诸如海马门区神经元等易损神经元中的快速诱导相比，短暂性脑缺血以延迟方式导致GFAP阳性星形胶质细胞中HSP 70表达。本研究结果可能为阐明缺血性神经元损伤机制提供线索。
