Chen J, Graham S H, Chan P H, Lan J, Zhou R L, Simon R P
Department of Neurology, University of California, San Francisco, USA.
Neuroreport. 1995 Jan 26;6(2):394-8. doi: 10.1097/00001756-199501000-00040.
Expression of the proto-oncogene bcl-2 prevents programmed cell death in vitro, but it is not known whether bcl-2 plays a role in determining cell survival after cerebral ischemia. Using immunohistochemistry and Western blot analysis, bcl-2 protein expression was studied in the rat brain 24 h following 60 or 120 min of temporary focal ischemia. Sixty minutes of ischemia induced bcl-2 protein in neurons throughout the frontoparietal cortex in non-infarcted regions, whereas 120 min of ischemia induced bcl-2 in neurons only just outside the margin of the infarction. bcl-2 protein was also induced in glial cells, mainly microglia, border zone of the infarction. In the infarcted regions of caudate and cortex, bcl-2 protein was exclusively induced in endothelial cells and the vessel walls. Western blot revealed a characteristic single band at 26 kDa only in ischemic samples. These data show that bcl-2 is induced in sublethally injured cells and suggest that bcl-2 could play a role in determining cell survival in cerebral ischemia.
原癌基因bcl-2的表达在体外可阻止程序性细胞死亡，但bcl-2在脑缺血后决定细胞存活方面是否起作用尚不清楚。运用免疫组织化学和蛋白质免疫印迹分析方法，研究了短暂性局灶性脑缺血60或120分钟后24小时大鼠脑内bcl-2蛋白的表达情况。60分钟的缺血在非梗死区域的整个额顶叶皮质神经元中诱导了bcl-2蛋白表达，而120分钟的缺血仅在梗死边缘外的神经元中诱导了bcl-2蛋白表达。在梗死灶边缘区的神经胶质细胞（主要是小胶质细胞）中也诱导了bcl-2蛋白表达。在尾状核和皮质的梗死区域，bcl-2蛋白仅在内皮细胞和血管壁中被诱导表达。蛋白质免疫印迹显示仅在缺血样本中出现一条26 kDa的特征性单带。这些数据表明，bcl-2在亚致死性损伤细胞中被诱导表达，提示bcl-2可能在脑缺血时决定细胞存活中发挥作用。
