Electroconvulsive seizure-induced VEGF is correlated with neuroprotective effects against cerebral infarction: Involvement of the phosphatidylinositol-3 kinase/Akt pathway
Electroconvulsive seizure-induced VEGF is correlated with neuroprotective effects against cerebral infarction: Involvement of the phosphatidylinositol-3 kinase/Akt pathway
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DOI：
10.1016/j.expneurol.2010.07.010
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发表时间：
2010-10-01
影响因子：
5.3
通讯作者：
Kobayashi, Hidenori
中科院分区：
文献类型：
--
作者：
Fujiki, Minoru;Abe, Eiji;Kobayashi, Hidenori
本研究证明了电惊厥刺激（ECS）作为一种潜在的神经保护性血管内皮生长因子（VEGF）诱导剂对缺血性损伤的细胞保护作用。磷脂酰肌醇-3 激酶/Akt (PI3K/Akt) 被认为是介导神经保护的重要因素。然而，ECS 后体内大脑的信号通路仍不清楚。我们测量并比较了梗塞体积，以研究 ECS 对大鼠大脑中动脉永久性闭塞引起的脑梗塞的影响。我们评估了 Wortmannin (Wort) 预处理的效果，Wortmannin 是一种针对 ECS 诱导的针对梗塞体积的神经保护的特异性 PI3K 抑制剂。为了阐明 PI3K/Akt 激活和神经保护之间的关系，我们使用免疫印迹分析来确定 ECS（有或没有麦芽汁处理）后存在的 p-Akt 和 VEGF 蛋白的量。 ECS（缺血前 6 小时用单一 ECS 预处理）的神经保护作用被麦芽汁预处理所阻止，这表明 PI3K/Akt 通路可能介导 ECS 依赖性保护。 ECS 诱导 p-Akt 和 VEGF，ECS 预处理增强缺血诱导的 VEGF，这两种情况均被麦芽汁预处理所阻止。这些结果表明，单一 ECS 诱导 p-Akt，并且 ECS 通过 VEGF 诱导在针对脑缺血的神经保护中发挥重要作用。 (C) 2010 Elsevier Inc. 保留所有权利。
The present study demonstrates the cytoprotective effect of electrical convulsive stimulation (ECS) as a potential neuroprotective vascular endothelial growth factor (VEGF) inducer against ischemic insult. Phosphatidylinositol-3 kinase/Akt (PI3K/Akt) is thought to be an important factor that mediates neuroprotection. However, the signaling pathways in the brain in vivo after ECS remain unclear. We measured and compared infarction volumes to investigate the effect of ECS on cerebral infarction induced by permanent middle cerebral artery occlusion in rats. We evaluated the effects of pretreatment with Wortmannin (Wort), a specific PI3K inhibitor of ECS-induced neuroprotection against infarction volumes. To clarify the relationship between PI3K/Akt activation and neuroprotection, we used immunoblot analysis to determine the amounts of p-Akt and VEGF proteins present after ECS with or without Wort treatment. Neuroprotective effects of ECS (pretreatment with a single ECS 6 h before ischemia) were prevented by Wort pretreatment, which indicates that the PI3K/Akt pathway may mediate ECS-dependent protection. ECS induced p-Akt and VEGF and ECS pretreatment enhanced ischemia-induced VEGF, both of which were prevented by Wort pretreatment. These results suggest that a single ECS induces p-Akt and that ECS plays an important role in neuroprotection against the cerebral ischemia through VEGF induction. (C) 2010 Elsevier Inc. All rights reserved.