摘要
目的探讨粒细胞集落刺激因子（G-CSF）动员自体造血干细胞对大脑中动脉栓塞，再灌注（McAo，R）大鼠细胞凋亡相关基因bcl-2、bax表达的影响。方法雄性SD大鼠90只分为模型组、模型＋G-CSF组、假手术组。评定神经病学评分；免疫组化双标记法鉴定造血干细胞向神经前体细胞分化；免疫组化法检测脑缺血后各时间点bcl-2、bax表达；原位末端标记法（TUNEL法）检测细胞凋亡。结果模型＋G-CSF组脑缺血24h时，缺血脑皮层及海马区出现CD34／nestin共标记细胞，48h共标记最为显著。与模型组比较，模型＋G-CSF组各时间点bcl-2表达增强，bax表达减弱，细胞凋亡率显著下降。结论大鼠自体造血干细胞可向神经前体细胞分化；G-GSF动员后，可能通过上调bcl-2和下调bax表达使脑缺血组织细胞凋亡率显著下降，并促进缺血脑组织修复。
Objective To study the effect of autologous hematopoietic stem cell （HSC） mobilized by granulocyte colony stimulating factor on the expression of bcl-2 and bax protein in focal cerebral ischemia/ reperfusion middle cerebral artery occlusion （MCAO/R） rats. Method Ninety male SD rats were divided into 3 groups： the model group, the G-CSF mobilized group and the control group. The neurological scale were evaluated. Immunohistochemisty and dual labeling technique were used to detect HSC differentiation to neuralward, and to detect the expressions of bcl-2 and bax protein in ischemia brain tissue at different time points. The cell apoptosis was determined by the TUNEL method. Results In the G-CSF treated group, at 24 hours after the ischemia/reperfusion injury, CD34 and nestin dual labeled cells were found in the ischemia brain; at 48 hours later, more dual labeled cells were observed. Compared with the model group, the expression of bcl-2 protein increased significantly, while the expression of bax protein attenuated. In contrast, the cell apoptosis declined significantly in the G-CSF treated group at different time points. Conclusion Autologous hematopoietie stem cells mobilized by G-CSF can differentiate into neuron-like cells. Inhibiting the cell apoptosis through upregulating the expression of bcl-2 protein and reducing the expression of bax protein may lead to the restoration of brain tissues after the ischemia/reperfusion injury.
出处
《中华急诊医学杂志》
CAS
CSCD
2007年第2期151-154,共4页
Chinese Journal of Emergency Medicine
基金
山东省自然科学基金资助课题（Y2003C07）
