The role of extracellular signal-regulated kinases in the neuroprotection of limb ischernic preconditioning
The role of extracellular signal-regulated kinases in the neuroprotection of limb ischernic preconditioning
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DOI：
10.1016/j.neures.2006.01.006
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发表时间：
2006-05-01
影响因子：
2.9
通讯作者：
Qi, Jie
中科院分区：
文献类型：
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作者：
Jin, Rui-Li;Li, Wen-Bin;Qi, Jie
为了阐明磷酸化细胞外信号调节激酶（pERK1/2）在大鼠肢体缺血预适应（LIP）神经保护中的作用，我们利用蛋白质印迹和流式细胞术研究了LIP后海马中pERK1/2的表达，以及pERK1/2抑制剂PD98059对LIP对正常诱导的CA1海马延迟性神经元死亡（DND）的神经保护作用的影响。严重的缺血性损伤。表明LIP后海马pERK1/2增加。在CA1海马中，ERK1/2激活在LIP后6小时开始增加，并在12小时达到峰值，并在LIP后5天降低至假手术水平。另一方面，在CA3/DG中，pERK1/2在1d时增强，在3cl时达到峰值，并持续至LIP后5d。在 LIP 之前用 PD98059 进行预处理，以剂量依赖性方式阻断了 LIP 的神经保护作用。这些发现支持 CA I 海马中 pERK 1/2 的上调有助于 LIP 对通常由脑缺血损伤引起的 DND 的神经保护作用。 (c) 2006 Elsevier Ireland Ltd 和日本神经科学学会。版权所有。
To clarify the role of phosphorylated extracellular signal-regulated kinases (pERK1/2) in the neuroprotection of limb ischemic preconditioning (LIP) in rats, we investigated the expression of pERK1/2 using Western blot and flow cytometry in the hippocampus after LIP and the effect of pERK1/2 inhibitor PD98059 on the neuroprotection of LIP against delayed neuronal death (DND) in the CA1 hippocampus normally induced by severe ischemic insult. It demonstrated that pERK1/2 in the hippocampus increased after LIP. In the CA1 hippocampus, ERK1/2 activation began to increase at 6 h and reached peak at 12 h after LIP, and decreased to sham level at 5 d after LIP. On the other hand, in the CA3/DG, pERK1/2 enhanced at I d, reached peak at 3 cl, and lasted to 5 d after LIP. Pretreatement with PD98059 before LIP blocked the neuroprotection of LIP in a dose-dependent manner. These findings supported that the upregulation of pERK 1/2 in the CA I hippocampus contributed to the neuroprotection of LIP against DND normally caused by the brain ischemic insult. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.