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作 者:赵旸[1] 于龙顺[2] 谭艳[2] 任世兰[2] 赵国举[2]
机构地区:[1]湖北十堰郧阳医学院研究生班学员现东汽花果医院儿科,442000 [2]郧阳医学院药理教研室
出 处:《中风与神经疾病杂志》1999年第6期331-334,共4页Journal of Apoplexy and Nervous Diseases
摘 要:目的探讨脑缺血复灌后连续应用GM1对改善记忆障碍的疗效。方法采用小鼠夹闭双侧颈总动脉的脑短暂缺血复灌模型.缺血15min后复灌开始即连续给予GM1,7d后进行开场行为、抑制性回避反应及Y-水迷宫试验.检测动物行为及认知功能.然后脑片观察海马CA1区锥体细胞密度。结果GM1组(10mg/Kg·d.共7d);抑制性回避反应经首次训练后24d再次检测,错误次数明显减少(从2.1±1.14到0.7±0.46)、Y-水迷宫试验正确次数明显增加(从0.7±0.9到1.5±1.0),而对照组两次检测结果均无显著差异。脑片观察GM1明显抑制脑缺血复灌后迟发性神经元死亡.GA1区锥体细胞数为78±15/mm。显著高于对照组(53±6.1/mm)。结论复灌开始后连续应用GM1治疗对脑缺血造成的记忆障碍有明显改善作用,这可能与其减少迟发性神经元死亡有关。Objective To study the improvement effects of GM_1 on brain ischemia reperfusion(BIR) induced memory impairment in mice. Method The reperfusion model following transient cerebral ischemia was produced by clamping both common carotid arteries in mice. Inhibitory avoidance response (IAR) and Y-water maze test methods were used to measure the changes of behavior and memory ability after 7d recirculation following 15 min ischemia. Brain slices were used to observe the changesof CA1 pyramidal cells density. Results GM1 (10mg /kg·d .ip for 7d) group:In IAR number of errorswas obviously decreased from 2.1±1.14 at training to 0.7±0.46 at retention test,and correct numberof Y-WMT was obviously increased from 0. 7±0. 9 to 1.5±1. 0. Control group were not changed significantly in The above test. GM1 inhibited the delayed neuronal death (DND) of hippocampus induced byBIR. CA1 pyramidal cells counts (78±15 /mm) was significantly higher than control group (53±6.1 /mm). Conclusion During recirculation treatment with GM1 exhibited a promising effect of improvementof memory impairment by BIR.and it may be related the reduction of DAD.
分 类 号:R743.310.6[医药卫生—神经病学与精神病学] R749.130.5[医药卫生—临床医学]
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