摘要:目的:探討加蘭他敏對急性酒精中毒大鼠海馬神經(jīng)元N甲基D天冬氨酸(NMDA)·R2B的影響。 方法:將60只大鼠分為對照組、酒精組及加蘭他敏組,每組各20只。酒精組以50％(v/v) 酒精12 mL/kg灌胃兩次/日,共7d。加蘭他敏組酒精(濃度、劑量同上)灌胃的同時(shí)腹腔注射加蘭他敏2mg/kg一次/日,共7d。對照組以等量生理鹽水灌胃。實(shí)驗(yàn)第8天取大鼠海馬區(qū)做蘇木精伊紅（HE）染色,觀察海馬區(qū)的病理學(xué)變化;免疫組織化學(xué)采用SABC法,觀察海馬區(qū)神經(jīng)元NR2B的表達(dá)。 結(jié)果: 病理學(xué)觀察結(jié)果：對照組海馬區(qū)神經(jīng)細(xì)胞排列整齊,胞質(zhì)淡染,無變性、壞死;酒精組神經(jīng)細(xì)胞層次不清、排列松散、細(xì)胞數(shù)量減少,部分細(xì)胞變性;加蘭他敏組神經(jīng)細(xì)胞層次較清、排列較密,細(xì)胞數(shù)目較酒精組增; 免疫組織化學(xué)結(jié)果：酒精組與對照組比較NR2B陽性表達(dá)細(xì)胞數(shù)量明顯減少(Plt;0.01);加蘭他敏組與酒精組比較NR2B陽性表達(dá)細(xì)胞數(shù)量明顯增高(Plt;0.05);加蘭他敏組與對照組比較NR2B表達(dá)細(xì)胞數(shù)量無明顯差異(Pgt;005)。 結(jié)論: 急性酒精中毒與海馬區(qū)神經(jīng)細(xì)胞的NR2B表達(dá)下調(diào)有關(guān);加蘭他敏具有保護(hù)急性酒精中毒導(dǎo)致的大鼠海馬區(qū)神經(jīng)細(xì)胞毒性的作用,其機(jī)制可能與加蘭他敏上調(diào)NR2B的表達(dá)有關(guān)。Abstract: Objective: To study the effects of galanthamine on NmethylDaspartic 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 HEstaining, 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 (Plt;0.01), increased in the galanthamine group than in the ethanol group (Plt;0.05), and had no difference between the galanthamin and control group (Pgt;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 upregulation NR2B expression.