中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (27): 5044-5047.doi: 10.3969/j.issn.1673-8225.2011.27.023

• 干细胞因子及调控因子 stem cell factors and regulatory factors • 上一篇    下一篇

粒细胞集落刺激因子对血管性痴呆大鼠海马神经细胞凋亡的影响

李肖云1， 兰希发2   

  1. 1秦皇岛市第三医院康复科， 河北省秦皇岛市 066000
    2河北医科大学附属秦皇岛市第一医院神经内科，河北省秦皇岛市 066000
  • 收稿日期:2010-12-13 修回日期:2011-01-13 出版日期:2011-07-02 发布日期:2011-07-02
  • 通讯作者: 兰希发，博士，主任医师，副教授，河北医科大学附属秦皇岛市第一医院神经内科，河北省秦皇岛市 066000 lanxifa2000@126.com
  • 作者简介:李肖云，女，1970年生，黑龙江省齐齐哈尔市人，汉族，黑龙江中医学院毕业，副主任医师，主要从事脑血管病的康复研究。

Effects of granulocyte colony-stimulating factor on neural cell apoptosis in the hippocampus of vascular dementia rats

Li Xiao-yun1, Lan Xi-fa2   

  1. 1Department of Rehabilitation, Qinhuangdao Third Hospital, Qinhuangdao  066000, Hebei Province, China
    2Department of Neurology, Qinhuangdao First Hospital Affiliated to Hebei Medical University, Qinhuangdao  066000, Hebei Province, China
  • Received:2010-12-13 Revised:2011-01-13 Online:2011-07-02 Published:2011-07-02
  • Contact: Lan Xi-fa, Doctor, Chief physician, Associate professor, Department of Neurology, Qinhuangdao First Hospital Affiliated to Hebei Medical University, Qinhuangdao 066000, Hebei Province, China lanxifa2000@126.com
  • About author:Li Xiao-yun, Associate chief physician, Department of Rehabilitation, Qinhuangdao Third Hospital, Qinhuangdao 066000, Hebei Province, China

PDF

590

被引次数

7

摘要：

背景：研究发现，粒细胞集落刺激因子可激活脑内成体神经干细胞，刺激其增殖和分化，还能促进脑内各种神经营养因子分泌，减小脑缺血动物模型的缺血灶，促进慢性脑卒中模型缺失神经功能的长期恢复。
目的：观察粒细胞集落刺激因子对血管性痴呆大鼠海马神经细胞凋亡的作用。
方法：采用永久性双侧颈总动脉结扎法建立大鼠血管性痴呆模型，抽签法随机分为4组：实验组(皮下注射粒细胞集落刺激因子干预治疗)、对照组(注射生理盐水)、假手术组(仅行颈前正中切开，不结扎颈总动脉)。采用Morris水迷宫进行定向航行观察大鼠逃避潜伏期，评价大鼠空间学习记忆能力，TUNEL染色和图像分析大鼠海马神经细胞的凋亡。
结果与结论：对照组和实验组大鼠脑缺血后7 d，大鼠平均逃避潜伏期较假手术组明显延长(P < 0.01)，海马组织TUNEL阳性凋亡细胞较假手术组显著增高(P < 0.01)，随着时间的延长，14，28 d时大鼠学习记忆功能障碍逐渐加重，相应海马组织TUNEL阳性凋亡细胞逐渐增加。14，28 d时实验组大鼠平均逃避潜伏期比对照组明显缩短，海马组织TUNEL阳性凋亡细胞也较对照组显著减少。说明脑缺血后早期给予外源性粒细胞集落刺激因子有助于减少海马组织神经细胞的凋亡，改善大鼠学习记忆能力。

关键词: 血管性痴呆, 海马, 神经细胞凋亡, 粒细胞集落刺激因子, 干细胞基础实验

Abstract:

BACKGROUND: The study found that granulocyte colony stimulating factor (G-CSF) can activate adult neural stem cells of the brain, stimulate their proliferation and differentiation, but also promote the secretion of varieties of neurotrophic factors of the brain, reduce ischemic lesions in the animal model of cerebral ischemia, and promote the long-term recovery of missing neurological function in chronic brain stroke models.
OBJECTIVE: To investigate the effect of G-CSF on the apoptosis of neural cells of the hippocampus of rats with vascular dementia.
METHODS: Rats were treated with a permanent bilateral occlusion of both common carotid arteries (2-VO) for establishing vascular dementia model. In the experimental group, the rats were given G-CSF by subcutaneous injection. In the control group, the rats were treated with saline. In the sham surgery group, an incision was made at midline of the neck, without ligation of common carotid artery. Morris water maze test was conducted to perform the oriented navigation and to observe escape latency in rats, and to assess the spatial learning and memory abilities. Neuronal cell apoptosis in the hippocampus of rats was investigated by TUNEL staining and image analysis.
RESULTS AND CONCLUSION: Compared with the sham surgery group, the average escape latency of rats was significantly longer in the control and experimental groups at 7 days following cerebral ischemia (P < 0.01). The number of TUNEL positive neurons in the hippocampus was significantly greater in the control and experimental groups compared with the sham surgery group (P < 0.01). With prolonged time, the learning and memory abilities became gradually severe and the number of TUNEL-positive cells gradually increased on days 14 and 28. The average escape latency of rats was significantly shorter in the experimental group compared with the control group on days 14 and 28. The number of TUNEL-positive cells in the hippocampus was significantly reduced in the experimental group compared with the control group. These indicated that treatment of exogenous G-CSF at early stage following cerebral ischemia contributes to the decrease in apoptosis of neural cells in the hippocampus and improves the learning and memory abilities in rats.

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