rhG—CSF对成年鼠持续低血流灌注海马损伤及认知障碍的改善作用

目的探讨rhG—CSF对持续低血流灌注成年鼠海马病理损伤及学习记忆障碍的改善作用。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10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区锥体细胞、凋亡细胞计数分析。结果缺血组整体逃逸时间显著高于对照组和干预组（P〈0．01）；缺血组停留于平台所在象限的时间显著少于对照组和干预组（P〈0．05）；缺血组跨过平台区域的次数显著少于对照组（P〈0．01）和干预组（P〈0．05）。缺血组海马CAl区NeuN阳性细胞显著少于对照组和干预组（P〈0．01）。缺血组凋亡细胞显著多于对照组（P〈0．01）和干预组（P〈0．05）。缺血组、对照组及干预组海马锥体细胞数量、凋亡细胞数量的变化分别与空间记忆功能改善呈正相关、负相关。结论持续低血流灌注脑缺血可致成年鼠学习记忆功能损害，rhG—CSF可通过促进海马锥体细胞增生、抑制细胞凋亡，来有效改善认知功能障碍。

Improvement of rhG - CSF on cognitive handicap and hippocampal injury in continuously cerebral hypoperfued adult rats

Objective To investigate improvement of rhG - CSF on cognitive handicap and hippocampal injury in continuously cerebral hypoperfued adult rats. Methods 30 male - SD - three - month rats were randomly divided into ischemic group, control group and rhG - CSF - treated group. Spatial learning and memory was accessed by Morris Water Maze, immunohistochemistry and immunofluorescence were employed to detected the number of NeuN positive cell and apoptosis in hippocmnpal CAI region. Results Escape latency of ischemic group rats was longer than control group and rhG - CSF - treated group （ P 〈 0.01 ）. Ischemic group rats spent less time in the platform quadrant than control group and rhG - CSF - treated group （ P 〈 0.05 ）. Times of ischemic group rats crossing the platform area was less than control group （ P 〈 0. O1 ） and rhG - CSF - treated group （ P 〈 0.05 ）. NeuN positive cells of ischemic group were significant less than control group and rhG - CSF - treated group （ P 〈 O. 01 ） in hippocampal CAI region. Apoptosis cells of ischemic group were more than control group （P 〈 0. 01 ） and rhG - CSF - treated group （ P 〈 0. 05 ）. Number of NeuN positive cells was positive related to spatial memory among ischemic group, control group and rhG - CSF - treated group. Number of apoptosis cells was negative correlation to spatial memory. Conclusion Spatial learning and memory is impaired in continuously cerebral bypoperfued adult rats, rhG - CSF can promote pyramidal cell hyperplasia and inhibite apoptosis, these are important pathological mechanism of cognition improvement.