粒细胞集落刺激因子动员骨髓干细胞治疗大鼠缺血性脑梗死

G-CSF mobilizes marrow stem cell to treat ischemia cerebral infarction in rats

目的 :探讨粒细胞集落刺激因子 (G -CSF)对大鼠缺血性脑梗死的治疗作用。方法 :采用线栓法制作大鼠缺血性脑梗死模型 ,1h后腹腔注射G -CSF 6 0 μg/kg。TTC、HE染色及免疫组化检测脑梗死灶体积、病理改变及CD34阳性细胞浸润情况。结果 :G -CSF治疗组大鼠脑梗死灶体积明显小于对照组 (P <0 0 1) ;其病理损伤程度较对照组轻 ;脑梗死部位出现CD34阳性单个核细胞浸润 ,并有CD34阳性呈锥状并且带有突起的神经样细胞生长 ,对照组未发现CD34阳性细胞。结论 :G -CSF可减轻大鼠缺血性脑梗死程度 ,减少脑梗死体积 ,其机理可能是G -CSF对缺血神经元具有保护作用 ,并动员自体骨髓干细胞 ,促进脑组织的再生与修复。

AIM: To explore whether granulocyte colony-stimulating factor (G-CSF) has the function of curing ischemia cerebral infarction in rats. METHODS: Rat cerebral infarction model was stablished by line occlusion and G-CSF 60 μg/kg was injected into abdominal cavity an hour later. The technique of TTC and HE staining and immunohistochemistry were used to detect the volume of infarction and pathological change and the infiltration of CD34 positive cells, respectively. RESULTS: The infarction volume of the rat brain was smaller in G-CSF-therapy group than infarction group 24 hours later and the pathological damage is slighter. Both CD34 positive mono-nucleus cells and CD34 positive neuron-like cells were detected in the rat brain of G-CSF-therapy group but not in the control one 24 hours later. CONCLUSIONS: G-CSF can relieve the ischemia degree and reduce the infarction volume. The possible mechanism is that G-CSF plays protection role on the ischemic neuron cells and moblizes stem cells in bone marrow, then stimulates the regeneration and plerosis of brain tissues.