右美沙芬对培养大鼠皮层神经元谷氨酸兴奋毒性和缺氧损伤的保护作用

Protection of Dextromethorphan against Hypoxic Injury and Excitoxicity of Glutamate in Cultured Rats Cortical Neurons

本文采用16～18d胎龄的大鼠皮层细胞进行分离培养，以培养上清液中乳酸脱氢酶（LDH）活性作为细胞损伤的指标，分别观察了缺氧和过量谷氨酸对皮层神经元的影响以及右美沙芬的保护作用。实验结果表明，外源性谷氨酸（10和50μmol／L）和缺氧（5h）均引起LDH释放增加，而这种作用皆被右美沙芬所抑制。提示右美沙芬对此有明显的保护作用。以上结果说明谷氨酸兴奋毒性与NMDA受体在缺血性脑损伤过程中起着重要的作用。

The effects of glutamate and anoxia on cultured cortical neurons from 16 to 18-day-old fetal rats and the protective effect of dextromethorphan (d-3-Methoxy-N-methylmorphinan ) were studied, and the cell damage was assessed by lactate dehydrogenase (LDH) release into culture medium. The results were as follows:Both exogenous glutamate(10 and 50μmol/L)and hypoxia (5h) induced LDH release, and this effect was inhibited by dextromethorphan. These results demonstratre that dextromethorphan may protect neurons from ischemia, suggesting that the neurotoxic effect of glutamate and NMDA (N-methyl-D-aspartate) receptors play an important role in the process of ischemia-induced damage in the brain.