Hara A, Iwai T, Niwa M, Uematsu T, Yoshimi N, Tanaka T, Mori H
Department of Pathology, Gifu University School of Medicine, Japan.
Brain Res. 1996 Mar 4;711(1-2):249-53. doi: 10.1016/0006-8993(95)01436-5.
Time-course expression of Bax and Bcl-2 proteins, identified as apoptosis-regulating molecules, was assessed in gerbil hippocampus following transient forebrain ischemia. Brain sections from animals sacrificed at 48, 72, 96 h and 7 days following 5 min ischemia were immunohistochemically evaluated using polyclonal antibodies specific for Bax and Bcl-2 proteins, respectively. The intensity of Bax expression in CA1 neurons increased with time and peaked at 72 h, and immediately disappeared at 96 h following 5 min ischemia. No expression of Bcl-2 in the CA1 neurons was recognized in all the time evaluated.
在沙土鼠短暂性前脑缺血后，对被确定为凋亡调节分子的Bax和Bcl-2蛋白的时间进程表达进行了评估。分别使用针对Bax和Bcl-2蛋白的多克隆抗体，对缺血5分钟后48、72、96小时和7天处死动物的脑切片进行免疫组织化学评估。CA1神经元中Bax表达强度随时间增加，在缺血5分钟后72小时达到峰值，并在96小时时立即消失。在所有评估时间内，均未在CA1神经元中检测到Bcl-2的表达。
