集落刺激因子对慢性脑缺血老龄鼠海马锥体细胞及认知功能的保护作用

The neuroprotection and cognition-amelioration after G-CSF treatment in chronic cerebral ischemic aged rats

目的观察粒细胞集落刺激因子(G-CSF)对慢性脑缺血老龄鼠认知障碍及海马锥体细胞的保护作用。方法 12个月龄雄性SD大鼠30只,随机分为造模组、对照组和干预组,每组10只。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。结果定位航行实验显示,造模组逃逸时间明显长于对照组和干预组(P<0.01);空间探索实验显示,造模组停留于平台所在象限的时间和跨过平台区域的次数明显少于对照组和干预组(P<0.01和P<0.05)。免疫组化染色显示,造模组海马CA1区NeuN阳性细胞明显少于对照组(P<0.01)和干预组(P<0.05)。荧光染色显示,造模组凋亡细胞明显多于对照组(P<0.01)和干预组(P<0.05)。造模组、对照组及干预组海马CA1区锥体细胞数量、凋亡细胞数量变化分别与空间记忆功能改善呈正相关、负相关。结论慢性脑缺血可致老龄鼠学习记忆能力受损,G-CSF可通过促进海马锥体细胞增生、抑制细胞凋亡实现对认知功能障碍的改善作用。

Objective To study the effect of granulocyte colony stimulating factor（G-CSF） on neuroprotection and cognition in chronic cerebral ischemia aged rats.Methods Thirty male SD twelve months rats were randomly divided into three groups of model（group A）,G-CSF treatment（group B） and control（group C） with 10 rats each.Spatial learning and memory ability was accessed by Morris water maze,immunohistochemistry and immunofluorescence were employed to detect neuron hyperplasia and apoptosis in the CA1 region.Results Escape latency in group A was longer than that in groups of B and C（P0.01）.The times for staying and crossing the platform area were less in group A than those in groups of B and C（P0.01 or P0.05）.NeuN positive cells of group A were less than those of groups of C and B in hippocampal CA1 region（P0.01 or P0.05）.Apoptosis cells of group A were more than those of groups of C and B（P0.01 or P0.05）.The number of NeuN positive cells was positively,but that of apoptosis cells was negatively,correlated to spatial memory improvement.Conclusion Spatial learning and memory abilities of chronic cerebral ischemic aged rats are impaired.G-CSF can improve rats cognition function through promoting pyramidal cell hyperplasia and inhibiting cell apoptosis.