摘要
探讨G GSF动员自体HSCs在大鼠MCAO R模型中分化为神经元样细胞的研究。采用大鼠大脑中动脉栓塞 再灌注 (MCAO R)模型 ,应用粒细胞集落刺激因子 (G GSF) ,促进骨髓造血干细胞 (HSCs)分裂增殖并向靶区“归巢” ,达到动员目的。观察大鼠神经病学评分 ,HE染色和免疫组化法观察病理改变及CD34、巢蛋白 (Nestin)阳性细胞的表达。模型大鼠脑缺血 再灌注后 2 4h时 ,大量淋巴、单核细胞浸润 ,脑缺血区少量Nestin细胞表达 ,无CD34+ 细胞表达。模型动员组 4 8h后 ,脑缺血区尤其是皮层缺血区大量CD34及Nestin阳性细胞表达 ,72h后CD34+ 细胞消失 ,但仍存在大量Nestin阳性细胞 ,且胞突增长 ;模型未动员组各时段未发现CD34+ 细胞 ,且Nestin阳性细胞明显少于动员组。结论 :应用G GSF可动员大鼠自体HSCs并向脑缺血区迁移 ,并可以分化为神经元前体细胞。
To investigate the differentiation of G-CSF mobilizing autologous bone marrow hematopoietic stem cells(HSCs) into neuron-like cells in focal cerebral ischemia/reperfusion(MCAO/R) rats. MCAO/R was induced with the filament occlusion method. Bone marrow stem cells were mobilized by Granulocyte colony-stimulating factor(G-CSF).The neurological scale was evaluated after focal cerebral ischemia. HE stain and immunohistochemisty were used to detect the pathologic change and the infiltration cells with positive expression of CD34 and Nestin in the regions of ischemia. In the G-CSF treatment group,24 hours after the focal cerebral ischemia/reperfusion injury,large number of infiltrative lymphocytes and myocytes were identified. Fourty-eight hours later, large number of CD34 and Nestin positive cells were found,72 hours later, CD34 positive cells disappeared,while the neuron-like cells with neurite outgrowth and Nestin expression were still existed and increased. In contrast,there was no CD34 cells and a few neuron-like cells with Nestin expression were found in the group without G-CSF mobilized. Autologous bone marrow hematopoietic stem cells mobilized by G-CSF can migrate into the region of ischemia and differentiate into neuron-like cells and restore the injured.
出处
《基础医学与临床》
CSCD
北大核心
2004年第3期310-313,共4页
Basic and Clinical Medicine
关键词
脑缺血
再灌注损伤
造血干细胞
粒细胞集落刺激因子
再生
cerebral ischemia/reperfusion
hematopoietic stem cells
granulocyte-colony-stimulating factor
regeneration
