Abe K, Saito H
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Neurosci Res. 1992 Jul;14(2):117-23. doi: 10.1016/0168-0102(92)90087-s.
The effects of epidermal growth factor (EGF) on glutamate-induced neuronal death were investigated in primary cultures of dissociated cerebellar neurons from fetal rats. Addition of an excess concentration of L-glutamate (5 mM) to the culture medium greatly decreased the number of surviving neurons 24 h later. When EGF was added to the culture medium 20 h prior to exposure to glutamate, glutamate-induced neuronal death was significantly reduced. The protective effects of EGF on glutamate neurotoxicity were concentration-dependent in the range of 0.01-10 ng/ml. When EGF was added 1 h prior to exposure to glutamate, it did not prevent glutamate-induced neuronal death, indicating that a longer exposure period is required for EGF to exert its protective effects. Furthermore, the protective effects of EGF on glutamate neurotoxicity disappeared in the presence of cycloheximide (0.1 microM), a protein synthesis inhibitor. These results suggest that EGF can protect brain neurons against glutamate toxicity through some protein synthesis.
在来自胎鼠的原代小脑神经元解离培养物中，研究了表皮生长因子（EGF）对谷氨酸诱导的神经元死亡的影响。向培养基中添加过量浓度的L-谷氨酸（5 mM），24小时后存活神经元的数量大大减少。当在暴露于谷氨酸之前20小时将EGF添加到培养基中时，谷氨酸诱导的神经元死亡明显减少。在0.01 - 10 ng/ml范围内，EGF对谷氨酸神经毒性的保护作用呈浓度依赖性。当在暴露于谷氨酸之前1小时添加EGF时，它并不能预防谷氨酸诱导的神经元死亡，这表明EGF需要更长的暴露时间来发挥其保护作用。此外，在蛋白质合成抑制剂环己酰亚胺（0.1 microM）存在的情况下，EGF对谷氨酸神经毒性的保护作用消失。这些结果表明，EGF可以通过一些蛋白质合成来保护脑神经元免受谷氨酸毒性的影响。
