›› 2014, Vol. 35 ›› Issue (11): 1296-1296.

• 论文 • 上一篇    下一篇

美金胺对大鼠脑缺血再灌注诱导学习记忆障碍的影响

陈超;张奉超   

  1. 江苏省徐州市儿童医院麻醉科,江苏 徐州,221000
  • 发布日期:2014-11-25

YANG Dong;WANG Qie;MI Liguo;ZHANG Yu

CHEN Chao;ZHANG Fengchao   

  • Published:2014-11-25

摘要: 目的:探讨美金胺对大鼠全脑缺血/再灌注(global cerebral ischemia/reperfusion,I/R)诱导学习记忆障碍的影响。方法通过4动脉结扎建立大鼠全脑缺血模型,在缺血后连续5 d腹腔注射美金胺,采用 Morris水迷宫进行行为学测定,通过焦油紫染色观察海马神经元的存活情况。结果与生理盐水对照组比较,假手术组和美金胺组逃逸潜伏期明显缩短(P<0.01);I/R组逃逸潜伏期明显长于假手术组和美金胺组(P<0.01),与生理盐水对照组差异无统计学意义(P>0.05);与生理盐水对照组比较,假手术组和美金胺组穿越平台时间、在原西北象限游泳的百分比和海马CA1区神经细胞数明显增多(P<0.01),而 I/R组穿越平台时间、在原象限游泳的百分比和海马区神经细胞较假手术组和美金胺组明显减少(P<0.01),但仍与生理盐水对照组比较差异无统计学意义(P>0.05)。结论美金胺可以改善大鼠全脑缺血再灌注所致的学习记忆障碍,该作用可能通过减轻缺血性神经元损伤实现。

关键词: 缺血再灌注损伤, 大鼠, 神经元, 记忆障碍

Abstract: Objective To investigate the effect of memantine on learning and memory disorder induced by cerebral ischemia/reperfusion (I/R)of rats.Methods Model of cerebral ischemia was established by the four-vessel occlusion method.Memantine was intraperitoneally inj ected for five days after the ischemia.Cresyl violet staining was used to observe the survival neurons in pyramidal cell layer of the hippocamal CA1 region and Morris water maze test was performed.Results Compared with those of saline control group, the escape latency of the orientation navigation experiment in sham group and memantine group was significantly shortened(P<0.01);the escape latency of I/R group was significantly longer than that of sham group and memantine group(P<0.01),but the escape latency of I/R group had no significant difference compared with that saline control group(P>0.05);Compared with those of control group,the crossing platform time,time percent of swimming in northwest and neuronal cell loss in hippocamal CA1 region in sham group and memantine group significantly raised(P<0.01),but the three items of I/R group significantly reduced in comparison with the above two groups(P<0.01),while they still had no significant differences compared with those of saline group(P>0.05).Conclusion Memantine can improve the learning and memory disorder induced by cerebral ischemia/reperfusion in rats through decreasing neuronal cell death.

Key words: reperfusion inj ury, rats, neurons, memory disordes

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