动员自体骨髓干细胞对大鼠脑缺血/再灌注损伤后bFGF表达的影响

目的探讨应用粒细胞集落刺激因子(G-CSF)动员自体骨髓干细胞对大鼠脑缺血/再灌注损伤后碱性成纤维细胞生长因子(bFGF)表达的影响。方法60只大鼠随机分为G-CSF治疗组及对照组,根据取样时间点的不同每组又分为7、14及21d3个亚组。采用线栓法制备大鼠大脑中动脉缺血/再灌注模型(MCAO/R),治疗组于MCAO/R后24h予G-CSF50μg·kg-1·d-1,连续5d,对照组皮下注射等量生理盐水。观察不同时间点大鼠的神经功能评分(NSS)。应用免疫组化法检测bFGF阳性细胞。结果大鼠脑缺血/再灌注后7、14、21d治疗组NSS分别为(4.0±0.9)分、(3.8±1.1)分、(3.5±1.3)分,对照组分别为(5.5±1.3)分、(5.8±1.4)分、(5.7±1.6)分,治疗组NSS明显优于对照组,差异有统计学意义(P<0.05)。2组大鼠脑缺血周边区均有bFGF免疫阳性细胞存在,并随时间延长而逐渐减少,bFGF阳性细胞计数(个/HP)显示术后7、14、21d治疗组分别为25.4±4.2、17.1±3.3、12.6±3.4,对照组分别为18.0±4.0、12.0±3.1、6.4±2.0,治疗组明显多于对照组(P<0.05),结论应用G-CSF动员自体骨髓干细胞治疗MCAO/R大鼠,可增加脑缺血后梗死边缘区bFGF的表达和改善神经功能。

The effect of mobilizing autologous bone marrow stem cells on the expression of bFGF in rats after cerebral ischemia/reperfusion

Objective To investigate the expression of basic fibroblast growth factor （bFGF） in mobilizing autologous bone marrow stem cells on focal cerebral ischemia/reperfusion in rats. Methods Sixty rats were divided randomly into the granulocyte colony stimulating factor （G-CSF） treatment group and control group. Both groups were divided again into 7 d, 14 d and 21 d subgroups according to the different time point. The MCAO/R model was induced with filament occlusion method, The treatment group was administrated G-CSF once a day for 5 days per 50μg/kg with hypodermic injection after model bulb. Yet the control group was applied with sodium chloride. The neurological severity scores （NSS） were evaluated in different time points. Immunohistochemistry technique was used to detect positive cells of bFGF. Results After MCAO/ R model built, the NSS of G-CSF group in 7 d, 14d and 21d was 4.0±0.9,3.8±1.1,3.5 ±1.3 respectively,the control group was 5.5 ±1.3, 5.8 ± 1.4 and 5.7 ±1.6 respectively. The NSS in treatment group was lower than the control group （ P 〈 0.05）. The positive cells of bFGF were detected in both G-CSF treatment group and control group, which situated in the marginal zone of the cerebral infarction, and gradually decreased along with time extends. The quantitative （per HP） statistical of bFGF positive cells in the G-CSF treatment group was 25.4 ± 4.2, 17. 1± 3.3 and 12.6 ± 3.4 respectively, and the control group was 18.0 ± 4.0, 12.0± 3. 1 and 6.4 ± 2.0. h showed that the positive bFGF cells in treatment group was higher than control group （ P 〈 0.05）. Conclusion It suggested that G-CSF could improve neural function and increase the expression of bFGF in marginal zone of the cerebral infaretion after cerebral ischemia/reperfusion in ratS.