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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 observe the protective effect of granulocyte-colony stimulating factor (G-CSF) on cognitive impairment and hippocampal pyramidal neurons in aged rats with chronic cerebral ischemia. Methods Thirty male SD rats, 12 months old, were randomly divided into model group, control group and intervention group, with 10 rats in each group. The Morris water maze test was used to evaluate the learning and memory function, the number of apoptotic cells in hippocampal CA1 pyramidal cells after immunostaining and fluorescent staining. Results The positioning navigation experiment showed that the escape time of the model control group was significantly longer than that of the control group and the intervention group (P <0.01). The space exploration experiments showed that the time spent by the model control group in the quadrant of the platform and the number of crossing the platform were significantly less than those of the control Group and intervention group (P <0.01 and P <0.05). Immunohistochemical staining showed that NeuN positive cells in hippocampal CA1 region of model group were significantly less than those of control group (P <0.01) and intervention group (P <0.05). Fluorescence staining showed that apoptotic cells in model group were significantly more than those in control group (P <0.01) and intervention group (P <0.05). The number of pyramidal cells and the number of apoptotic cells in CA1 area of hippocampus in model group, control group and intervention group were positively correlated and negatively correlated with the improvement of spatial memory function respectively. Conclusions Chronic cerebral ischemia can impair the ability of learning and memory in aged rats. G-CSF can improve the cognitive dysfunction by promoting hippocampal pyramidal cell proliferation and inhibiting apoptosis.