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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<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<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>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。
Objective: To investigate the effects of galantamine on N-methyl-D-aspartate (NMDA) · R2B in hippocampal neurons of rats with acute alcoholism. Methods: 60 rats were divided into control group, alcohol group and galantamine group, 20 rats in each group. Alcohol group with 50% (v / v) alcohol 12 mL / kg gavage twice daily for 7 days. Galantamine group alcohol (concentration, dose ibid) intragastric administration of galantamine 2mg / kg once daily, a total of 7d. Control group with the same amount of saline gavage. On day 8, hematoxylin and eosin (HE) staining was performed in hippocampus of rats to observe the pathological changes of hippocampus. SABC immunohistochemistry was used to observe the expression of NR2B in hippocampal neurons. Results: The results of pathology showed that the neurons in the hippocampus of the control group were arranged neatly, the cytoplasm was lightly stained, no degeneration and necrosis. The level of neuronal cells in the alcohol group was unclear, the arrangement was loose, the number of cells decreased and some cells degenerated. The numbers of NR2B positive cells in alcohol group were significantly decreased compared with those in control group (P <0.01), while those in galanthamine group and alcohol group were significantly lower than those in alcohol group The number of NR2B positive cells was significantly increased (P <0.05). There was no significant difference in NR2B expressing cells between galanthamine group and control group (P> 0.05). CONCLUSION: Acute alcoholism is related to the down-regulation of NR2B expression in hippocampal neurons. Galantamine has the protective effect on the neurotoxicity in hippocampus induced by acute alcoholism, which may be related to the upregulation of NR2B expression by galanthamine .