Extracellular signal-regulated kinase 1/2 activation in hippocampus after cerebral ischemia may not interfere with postischemic cell death
Extracellular signal-regulated kinase 1/2 activation in hippocampus after cerebral ischemia may not interfere with postischemic cell death
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DOI：
10.1016/s0006-8993(01)02275-2
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发表时间：
2001-05-18
期刊：
影响因子：
2.9
通讯作者：
Zhang, CY
中科院分区：
文献类型：
--
作者：
Gu, ZL;Jiang, Q;Zhang, CY
为了研究细胞外信号调节激酶 112 (ERK1/2) 的激活对脑缺血损伤的影响，检查了海马中活性（二磷酸化）ERK1/2 免疫反应性的时空变化。 Western blot显示二磷酸化ERK1/2在脑缺血10分钟时下降，但在再灌注期间迅速（2分钟内）和短暂（4小时内）上升。免疫组织化学显示缺血后CA1锥体细胞体中几乎没有观察到二磷酸化的ERK1/2免疫反应性。而 CA3/DG 的神经元以及 CA1 和 CA3 区域的纤维系统中均观察到强烈的免疫反应性。脑室输注ERK激酶特异性抑制剂PD98059，完全阻止缺血后ERK1/2的激活，但对CA1亚区锥体细胞的存活没有影响。结果表明，脑缺血后海马中ERK 112的激活可能不会干扰CA1区缺血后的细胞死亡。 (C) 2001 Elsevier Science B.V. 保留所有权利。
To investigate the effect of the activation of extracellular signal-regulated kinase 112 (ERK1/2) on cerebral ischemic injury, temporospatial alterations of active (diphosphorylated) ERK1/2 immunoreactivity in hippocampus was examined. Western blot showed that diphosphorylated ERK1/2 were decreased at 10 min of cerebral ischemia but increased rapidly (within 2 min) and transiently (within 4 h) during reperfusion. Immunohistochemistry showed that little diphosphorylated ERK1/2 immunoreactivity was seen in CA1 pyramidal cell bodies after ischemia. while strong immunoreactivity were seen in neuronal bodies in CA3/DG and in fiber systems in both CA1 and CA3 regions. Cerebral ventricular infusion of PD98059, a specific inhibitor of ERK kinase, completely prevented ERK1/2 activation after ischemia but had no effect on the survival of pyramidal cells in CA1 subfield. The results suggest that ERK 112 activation in hippocampus after brain ischemia may not interfere with the postischemic cell death in CA1 region. (C) 2001 Elsevier Science B.V. All rights reserved.