集落刺激因子对慢性脑缺血成年鼠胶质细胞可塑性及记忆改善的影响  

Treatment effects of GCSF on gliacyte plasticity and cognitive function in chronic cerebral hypoperfued adult rats

作　　者：舒细记[1] 柳威[1] 周红艳[1] 熊巍鹏[1] 陈艳华[1] 艾永循[1] 

机构地区：[1]江汉大学医学院病理学与病理生理学教研室,430056

出　　处：《中国实用医药》2010年第32期8-9,共2页China Practical Medicine

摘　　要：目的探讨rhG-CSF对慢性低血流灌注脑缺血成年鼠海马胶质细胞可塑性及记忆改善的影响。方法 3月龄雄性SD大鼠随机分为缺血组、对照组和干预组,每组15只。采用Morris水迷宫实验评估大鼠学习记忆功能,免疫组化及荧光染色后对海马CA1区胶质细胞数量及胞质突起长度进行图像分析。结果缺血组海马CA1区GFAP阳性细胞明显少于对照组(P<0.01)和干预组(P<0.05)。缺血组GFAP阳性细胞胞质突起长度明显低于对照组和干预组(P<0.05)。缺血组逃逸时间明显高于对照组和干预组(P<0.01);缺血组大鼠在平台象限的停留时间明显少于对照组和干预组(P<0.05);缺血组跨过平台区域的次数明显少于对照组(P<0.01)和干预组(P<0.05)。缺血组、对照组及干预组海马CA1区胶质细胞的数量、胞质突起长度与空间记忆改善均呈正相关。结论 rhG-CSF促进海马胶质细胞可塑性改变,是慢性脑缺血成年鼠记忆功能改善的重要病理修复机制。Objective To explore effect of rhG-CSF on gliacyte plasticity and cognitive handicap in chronic cerebral hypoperfusion adult rats.Methods 45 male-SD-three-month rats were randomly divided into ischemic model group,control group and rhG-CSF-treated group,each group has 15 rats.Spatial learning and memory was accessed by Morris Water Maze,immunohistochemistry and image analysis were employed to detected the number and cytoplasmic process length of GFAP positive cell in hippocampal CA1 region.Results GFAP positive cells of ischemic model group was significant less than control group（P 0.01） and rhG-CSFtreated group（P 0.05）.The cytoplasmic process length of GFAP positive cell of ischemic model group was significant less than control group and rhG-CSF-treated group（P 0.05）.Escape latency of ischemic model group rats was longer than control group and rhG-CSF-treated group（P 0.01）.Ischemic model group spent less time in the platform quadrant than control group and rhG-CSF-treated group（P 0.05）.As for number of crossing the platform area,ischemic model group was less than control group（P 0.01） and rhG-CSF-treated group（P 0.05）.Number and the cytoplasmic process length of glia cells were positive related to spatial learning among ischemic model group,control group and rhG-CSF-treated group.Conclusion rhG-CSF can enhance congnitive function by promoting gliacyte plasticity.The alteration of gliacyte plasticity may be an important pathologic mechanism of cognition improvement.

关 键 词：慢性脑缺血 粒细胞集落刺激因子 胶质细胞可塑性 学习记忆 海马 

分 类 号：R749.1[医药卫生—神经病学与精神病学]