【摘要】 目的:探讨酒精导致大脑损伤的机制。方法:建立小鼠慢性酒精中毒的动物模型,观察动物行为学的改变,测量血浆酒精浓度,进行Morris水迷宫测定,通过组织免疫荧光技术和Western Blot方法,进行大脑组织SNAP-25的定位和定量检测。结果:酒精处理组的小鼠血浆酒精浓度达到中毒浓度,Morris水迷宫试验潜伏期延长。SNAP-25定位于细胞的胞浆内,酒精处理组的含量明显地较对照组减少。结论:SNAP-25参与了慢性酒精中毒大脑损伤的机制。更多还原

【Abstract】 Objective:To explore the mechanisms how ethanol leads to brain injury.Methods:We built chronic ethanol intoxication model of mice by freely drinking ethanol solution,observed behavioral changes and measured latency of Morris maze,ethanol concentrations in plasma,manifested the localization and compared the content of SNAP-25 in homogenate of brain by histological immunofluorescence staining and Western blot method,respectively.Results:The plasma ethanol concentration of ethanol treatment group was high enough for chronic intoxication and the latency of Morris maze was longer than that of control group.SNAP-25 was localized in cell plasma and the content of SNAP-25 in homogenate of brain in ethanol treatment group was higher than those in control group.Conclusion: SNAP-25 is involved in the mechanism of brain injury of chronic ethanol intoxication.更多还原