摘要
背景:半乳凝素1表达于室管膜下区的星形胶质细胞中并诱导其分化,分化的星形胶质细胞可明显提高脑源性神经生长因子的产生。目的:观察侧脑室注入半乳凝素1对脑缺血损伤大鼠内源性神经干细胞增殖、迁移的影响。设计、时间及地点:细胞学体内观察实验,于2007-03/11在佳木斯大学神经科学研究所完成。材料:纯种清洁级成年Wistar大鼠48只,随机分为模型组、药物组,24只/组。半乳凝素1为北京晶美生物工程公司产品。方法:两组大鼠均采用线栓法制作局灶性大脑中动脉闭塞模型。造模后24h,药物组经右侧侧脑室注入10μL浓度为0.2g/L的半乳凝素1,模型组注射等量生理盐水。分别于缺血再灌注后3,7,14,28d处死大鼠,取脑组织制作石蜡切片,处死前1d腹腔注射BrdU。主要观察指标:免疫组织化学染色检测大脑室管膜下区BrdU和巢蛋白阳性细胞的表达。结果:模型组缺血再灌注3d后大脑室管膜下区BrdU、巢蛋白阳性细胞开始增加,7d增殖达高峰,14d后表达开始下降,28d后下降至最低。药物组缺血再灌注3d后大脑室管膜下区两种阳性细胞均明显增加;7d增殖达高峰,半定量分析BrdU、巢蛋白阳性细胞数分别是模型组的2倍和1.5倍,且BrdU阳性细胞向腹外侧迁移,巢蛋白阳性细胞胞体变大,突起增长,并有向外侧迁移进入脑实质的迹象;14d后开始下降;28d降至最低,但仍明显多于模型组(P<0.05)。结论:经侧脑室注入半乳凝素1在大鼠脑缺血后可激活内源性神经干细胞原位增殖,并存在由增殖区向外周脑实质迁移的趋势。
BACKGROUND： Galectin-1 （semi-latex agglutination-1） is detected in astrocytes in the subependymal region, and induces differentiation of astrocytes. Differentiated astrocytes significantly elevates production of brain-derived neurotrophic factor. OBJECTIVE： To investigate effects of Galectin-1 injection into the lateral ventricle of rats on proliferation and migration of endogenous neural stem cells following ischemic injury. DESIGN, TIME AND SETTING： The cytology in vivo observation experiment was performed at the Institute of Neuroscience of Jiamusi University from March to November 2007. MATERIALS： A total of 48 clean adult Wistar rats were selected and randomly assigned into a model group and a drug group, with 24 in each group. Galectin- 1 was obtained from Beijing Jingmei. METHODS： Rat models of focal middle cerebral artery occlusion were established by the thread method in both groups. At 24 hours after model establishment, 10 μ L 0.2 g/L Galectin-1 were infused into the right lateral cerebral ventricle of rats in the drug group, and equal volume of saline was injected into rats in the model group. Rats were killed at 3, 7, 14 and 28 days following ischemia/reperfusion. Brain tissues were obtained, sliced and embedded in paraffin. BrdU was intraperitoneally injected into rats at 1 day prior to killing. MAIN OUTCOME MEASURES： Immunohistochemistry was used to detect BrdU, Nestin expression in the brain subependymal region. RESULTS： In the model group, Nestin and BrdU-positive cells began to increase in the subependymal region at 3 days, and reached a peak at 7 days, but decreased at 14 days and reduced to a minimal levels at 28 days after ischemia/reperfusion. In the drug group, Nestin and BrdU-positive cells significantly increased in the subependymal region at 3 days, reached a peak at 7 days after ischemia/reperfusion. Semiquantitative analysis demonstrated that number of Nestin and BrdU-positive cells in the drug group was respectively 2 times and 1.5 times compared with the model group. BrdU-positive cells migrated to ventrolateral region. Nestin-positive cells became bigger in size, with increased processes, and migrated to lateral region towards the brain parenchyma. Nestin and BrdU-positive cells in the drug group decreased at 14 days and reduced to a minimal levels at 28 days, which still more than in the model group （P 〈 0.05）. CONCLUSION： Galectin-1 injected into the lateral cerebral ventricle can activate endogenous neural stem cells in situ proliferation following rat cerebral ischemia, which has a tendency of migration from proliferative zone to peripheral brain parenchyma.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
北大核心
2008年第38期7487-7490,共4页
Journal of Clinical Rehabilitative Tissue Engineering Research
基金
黑龙江省自然科学基金(D2004-16)~~
