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Effects of the Galanthamine on NMDAR2B of Hippocampus Neuron in Acute Alcoholism of Rats

摘要:目的:探讨加兰他敏对急性酒精中毒大鼠海马神经元N甲基D天冬氨酸(NMDA)·R2B的影响。 方法:将60只大鼠分为对照组、酒精组及加兰他敏组,每组各20只。酒精组以50％(v/v) 酒精12 mL/kg灌胃两次/日,共7d。加兰他敏组酒精(浓度、剂量同上)灌胃的同时腹腔注射加兰他敏2mg/kg一次/日,共7d。对照组以等量生理盐水灌胃。实验第8天取大鼠海马区做苏木精伊红（HE）染色,观察海马区的病理学变化;免疫组织化学采用SABC法,观察海马区神经元NR2B的表达。 结果: 病理学观察结果：对照组海马区神经细胞排列整齐,胞质淡染,无变性、坏死;酒精组神经细胞层次不清、排列松散、细胞数量减少,部分细胞变性;加兰他敏组神经细胞层次较清、排列较密,细胞数目较酒精组增; 免疫组织化学结果：酒精组与对照组比较NR2B阳性表达细胞数量明显减少(Plt;0.01);加兰他敏组与酒精组比较NR2B阳性表达细胞数量明显增高(Plt;0.05);加兰他敏组与对照组比较NR2B表达细胞数量无明显差异(Pgt;005)。 结论: 急性酒精中毒与海马区神经细胞的NR2B表达下调有关;加兰他敏具有保护急性酒精中毒导致的大鼠海马区神经细胞毒性的作用,其机制可能与加兰他敏上调NR2B的表达有关。Abstract: Objective: To study the effects of galanthamine on NmethylDaspartic acid receptor 2B (NMDAR2B, NR2B) in the hippocampus (HIP) of acute alcoholism rats. Methods: Total of 60 wistar male rats were randomly divided into control group, ethanol group and glanthamine group, and there were 20 rats in each group. The rats in ethanol group were given by intragastric administration with 50% alcohol (v/v) on the dose of 12 ml/kg twice per day, in control group were given by same dose of saline, and in galanthamine group were treated by intragastric administration with the same concentration and dosage of alcohol as in ethanol group and peritoneal injection with 2 mg/kg of galanthamine once per day for 7 days. In eighth day of experiment, the rats were sacrificed under etherization, and pathological changes of HIP’s zone of rat were observed by HEstaining, and expression of NR2B in neurons of HIP’s zone by immunohistochemical SABC method. Results: The results observed by histopathology showed that in control group, neurons of HIP’s zone lined up in order, cytoplasm had faint staining, and were no degeneration and necrosis; in ethanol group, nerve cells’ layer was unclear, structure was loose, cell number reduced and part of cells degenerated; in galanthamine group, layer of neurons was comparatively clear and arrangement was comparatively dense, and the cell number increased obviously more than ethanol group. The results detected by Immunohistochemistry for NR2B showed that the cell number with expression of NR2B in the HIP’s zone decreased significantly in the ethanol group than in the control group (Plt;0.01), increased in the galanthamine group than in the ethanol group (Plt;0.05), and had no difference between the galanthamin and control group (Pgt;0.05). Conclusion: Acute alcoholism may relate to down regulation of expression of neuron’s NR2B in HIP’s zone;The galanthamin has role of protection for neuron in HIP’s zone induced by toxicity of acute alcoholism, and its mechanism may relate to galanthamin upregulation NR2B expression.