纳洛酮对神经元GluR2表达的影响及缺氧损伤保护作用

目的：研究纳洛酮对缺氧损伤神经元膜表面AMPA（amino-3-hyoroxy-5-methylisoxazole-4-propionicacid，α-氨基-3-羟基-5甲基-4-异噁唑丙酸）受体在谷氨酸受体第二亚单位（GluR2，glutamic acid receptor 2）表达的影响及其对神经细胞凋亡的保护作用。方法：取体外培养12d的大鼠海马神经元，建立缺氧再灌注损伤模型，分别采用流式细胞和双重免疫荧光技术定量观察神经元凋亡数量、胞膜表面GluR2含量变化及纳洛酮的调节作用。结果：纳洛酮可上调缺氧损伤后神经元膜GluR2的含量（P〈0.05），减少缺氧诱导的神经元凋亡的数量（P〈0.01）。结论：纳洛酮通过上调神经元膜表面GluR2含量，减少神经元凋亡，减轻继发性脑损害。

Regulative Effect of Naloxone on Neural GIuR2 Expression and Its Protection against Ischemic Injuries

Objective:To investigate the effect of naloxone on the neural surface GluR2 expression and its protection anti-apoptosis of neuron by anoxia.Methods:Hippocampus neurons cultured for 12 days were used to establish the ischemia and reperfusion model.The neuron apoptosis,surface GluR2 expression and the regulation of naloxone were quantitatively measured with fluid cytometer and double immunofiuorescence labeling techniques respectively.Results:Compared with the control group,the neural surface GluR2 expression after ischemic insult could be significantly upregulated with naloxone treatment(P<0.05),and the amount of apoptosis neurons was significantly decreased(P<0.01).Conclusion:Naloxone can reduce the amount of apoptosis cells and extenuate the secondary injury after ischemic insult by up-regulating the surface GluR2 expression of neuron.