纳洛酮对神经元GluR2表达的影响及缺氧损伤保护作用  

Regulative Effect of Naloxone on Neural GluR2 Expression and Its Protection against Ischemic Injuries

作　　者：姜利人[1] 陈力学[2] 刘宝松[2] 

机构地区：[1]解放军第二五一医院,河北张家口075000 [2]第三军医大学大坪医院野战外科研究所创伤烧伤与复合伤国家重点实验室,重庆400042

出　　处：《中国误诊学杂志》2007年第19期4445-4447,共3页Chinese Journal of Misdiagnostics

基　　金：教育部留学回国人员科研启动基金资助(编号:2005-383)

摘　　要：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-异口恶唑丙酸)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12 d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。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 immuno-fiuorescence labeling techniques respectively. Results： Compared with the control group, the neural surface GluR2 expression after isehemic 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.

关 键 词：纳洛酮/药理学 再灌注损伤/药物疗法/病理学/代谢 受体 AMPA/代谢/药物作用 神经元/细胞学/药物作用 细胞凋亡/药物作用 动物 体外研究 

分 类 号：R96[医药卫生—药理学] R349.12[医药卫生—药学]