骨髓单个核细胞对急性脑缺血小鼠模型的保护作用及机制

Research for the antiapoptotic mechanisms of bone marrow mesenchymal stem cells in the treatment of brain ischemia stroke

目的 探讨骨髓单个核细胞（BMMCs）移植对急性脑缺血小鼠脑组织细胞的凋亡保护作用.方法 从骨髓中分离BMMCs,体外扩大培养后流式细胞术鉴定细胞表面标志物,将鉴定好的BMMCs移植入构建的小鼠脑缺血再灌注模型（MACO）中,通过Tunel染色及Western印迹检测细胞凋亡及凋亡相关分子caspase的变化.免疫组织荧光及Western印迹检测血管内皮细胞修复相关分子eNOS、ICAM-1、CD31的表达情况.结果 BMMCs移植到小鼠脑缺血模型后,BMMCs细胞治疗组细胞凋亡数量（12.8±3.0）明显低于MACO级（78.2±1.4）,eNOS、CD31表达增高[（80.0±6.2）比（31.2±1.6）;（85 ±3）比（45±5）;P＜0.01],ICAM-1表达下降[（34.1±2.2）比（85.2±2.8）,P＜0.01].结论 BMMCs可通过调节血管内皮细胞修复相关分子的表达减少缺血后细胞的凋亡.

Objective To evaluate the anti-apoptosis role of bone marrow mesenchymal stem cells （BMMCs） transplantation to cell cerebral brain ischemia mice.Methods BMMCs were separated through Ficoll from bone marrow,after amplified in vitro,flow cytometry was used to identify the surface markers.Then cells were transplanted into Middle cerebral artery occlusion（MACO） mice,in situ cell death detection kit and Western blot were used to examine the cell apoptosis.Immunofluorescence and Western blot were used to detect the expression of eNOS,ICAM-1,CD31 which are related to the repair of vascular endothelial cells.Results After BMMCs transplantation,the number of apoptosis cells was decreased from （78.2 ± 1.4） to （12.8±3.0）,P〈0.05.The expression of eNOS （80.0±6.2 vs31.2±1.6,P〈0.01） and CD31 （85 ± 3 vs 45 ± 5,P 〈0.01）,were higher than MACO,while ICAM-1 was lower than MACO （34.1 ± 2.2 vs 85.2 ± 2.8,P 〈 0.01）.Conclusion BMMCs reduce the cell apoptosis of ischemia mice through regulate the expression of vascular endothelial cells relate genes.