Prakasa Babu P, Yoshida Y, Su M, Segura M, Kawamura S, Yasui N
Department of Pathology, Research Institute for Brain and Blood Vessels-Akita, Senshu Kubota Machi, 6-10, 010-0874, Akita, Japan.
Neurosci Lett. 2000 Sep 22;291(3):196-200. doi: 10.1016/s0304-3940(00)01404-x.
Recent studies suggest that mild hypothermia significantly alleviate damage following cerebral ischemia though the precise mechanism is poorly defined. In the present study, middle cerebral artery occlusion (MCAo) was induced in Sprague-Dawley (SD) rats for 1 h followed by varying periods of reperfusion. Cerebral infarcts identified by hematoxylin & eosin (H&E) staining revealed extensive lesion in normothermic (NT) 37 degrees C and small lesion in hypothermic (HT) 33 degrees C group of rats. Immunohistochemical analysis revealed Bcl-2 was induced in many neurons of HT group, while Bax and cytochrome c was induced in few neurons. In situ detection of DNA fragmentation using 3'-OH end labeling method (terminal dUTP nick-end labelling (TUNEL)) indicated, higher number of TUNEL-positive cells in NT group, but significantly decreased in HT group. The expression pattern revealed many neurons at the penumbra region could survive in HT group whereas, many neurons are committed to die in NT group. Our results suggest that hypothermia is selectively interfering at more than one place and providing protection.
近期研究表明，轻度低温可显著减轻脑缺血后的损伤，尽管确切机制尚不清楚。在本研究中，对Sprague-Dawley（SD）大鼠进行大脑中动脉闭塞（MCAo）1小时，随后进行不同时长的再灌注。通过苏木精和伊红（H&E）染色鉴定的脑梗死显示，在体温正常（NT）37摄氏度的大鼠组中出现广泛损伤，而在体温降低（HT）33摄氏度的大鼠组中损伤较小。免疫组织化学分析显示，HT组的许多神经元中诱导产生了Bcl-2，而Bax和细胞色素c仅在少数神经元中诱导产生。使用3'-OH末端标记法（末端脱氧尿苷三磷酸缺口末端标记法（TUNEL））原位检测DNA片段化表明，NT组中TUNEL阳性细胞数量较多，而HT组中显著减少。表达模式显示，HT组中半暗带区域的许多神经元能够存活，而NT组中的许多神经元则注定死亡。我们的结果表明，低温在多个部位发挥选择性干预作用并提供保护。
