Neuroprotective effects of neuregulin-1 on B35 neuronal cells following ischemia
Neuroprotective effects of neuregulin-1 on B35 neuronal cells following ischemia
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DOI：
10.1016/j.brainres.2008.02.059
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发表时间：
2008-05-19
期刊：
影响因子：
2.9
通讯作者：
Ford, Byron D.
中科院分区：
文献类型：
--
作者：
Croslan, DaJoie R.;Schoell, Matthew C.;Ford, Byron D.
我们先前表明，神经调节蛋白-1（NRG-1）保护神经元免于局灶性缺血后的体内死亡。本研究的目的是建立一个体外大鼠缺血模型，以检查参与NRG-1对缺血诱导的神经元死亡的神经保护作用的细胞和分子机制。大鼠B-35神经母细胞瘤细胞分化血清撤退，发展增强的神经元特性，包括，神经突延伸和上调的神经元分化标志物。当B35神经元进行氧葡萄糖剥夺（OGD）/复氧或谷氨酸，广泛的神经元死亡后，这两种治疗。在OGD后立即用NRG-1处理显著增加神经元存活。NRG-1给药还导致膜联蛋白V（细胞凋亡的早期标志物）显著减少。然而，谷氨酸的神经毒性作用不受NRG-1的影响。NRG-1的神经保护作用被磷脂酰肌醇-3-激酶/Akt通路的抑制剂阻止。这些结果为深入了解NRG-1保护神经元免受缺血性脑损伤的机制提供了新的模型。(C)2008 Elsevier B. V.保留所有权利。
We previously showed that neuregulin-1 (NRG-1) protected neurons from death in vivo following focal ischemia. The goal of this study was to develop an in vitro rat ischemia model to examine the cellular and molecular mechanisms involved in the neuroprotective effects of NRG-1 on ischemia-induced neuronal death. Rat B-35 neuroblastoma cells differentiated by serum withdrawal, developed enhanced neuronal characteristics including, neurite extension and upregulation of neuronal markers of differentiation. When B35 neurons were subjected to oxygen glucose deprivation (OGD)/reoxygenation or glutamate, widespread neuronal death was seen after both treatments. Treatment with NRG-1 immediately after OGD significantly increased neuronal survival. NRG-1 administration also resulted in a significant decrease in annexin V, an early marker of apoptosis. However, the neurotoxic actions of glutamate were unaffected by NRG-1. The neuroprotective effects of NRG-1 were prevented by an inhibitor of the phosphatidylinositol-3-kinase/Akt pathway. These results provide a new model to gain insight into the mechanisms employed by NRG-1 to protect neurons from ischemic brain injury. (C) 2008 Elsevier B.V. All rights reserved.