体内心肌微环境诱导骨髓干细胞分化的研究

Study on Bone Marrow Stem Cells Induced in Myocardium Micro-condition in vivo

目的 :了解干细胞动员剂动员的骨髓干细胞的心肌细胞分化潜能及对缺血心肌的影响。方法 :采用异丙肾上腺素(ISO)皮下注射制作大鼠心肌梗死模型 ,联用粒细胞集落刺激因子 (G CSF)和低分子量硫酸葡聚糖动员大鼠自体骨髓干细胞释放和迁移至心肌梗死灶 ,于用ISO后 2 4、 4 8h、 2周杀死大鼠 ,取出心脏 ,通过免疫组化、苏木精 伊红染色和VanGieson s苦味酸性复红染色方法观察大鼠心肌梗死灶的CD34+ 细胞的浸润及心肌再生、心肌纤维化的情况。结果 :用ISO后 2 4h ,动员组大鼠心肌梗死区可见CD34+ 细胞浸润 ,并有CD34+ 新生心肌细胞生长 ;2周后瘢痕组织少 ,心肌纤维化程度轻 ,缺血心肌基本结构得到保护。结论 :急性心肌梗死发生后 ,联用G CSF和低分子量硫酸葡聚糖能迅速动员自体骨髓干细胞向心肌梗死灶内迁移、存活和向心肌细胞、血管内皮细胞等分化 。

Objective:To investigate the potential of differentiating to myocytes of the granulocyte colony-stimulating factor(G-CSF)and dextran sulfate sodium salt-mobilized bone marrow stem cells.Methods:After injection of isoprenaline(ISO) ip.to develop acute ischemic model, rat bone marrow stem cells were mobilized by G-CSF and dextran sulfate sodium salt and migrated to the site of myocardial infarction.Hearts were harvested from 24 hours to 2 weeks after administration of ISO for histopathological examination.Immunohistochemisty,Hematoxylin-eosin staining and Van Giesons staining(VG)were used to detect infiltration of CD34 +monocytes and the regeneration of myocytes and the inhibition of fibroatrophy of ischemic myocardium.Results:Twenty-four hours after administration of ISO,a large amount of infiltrative monocytes and regenerative myocytes which were CD34 + expression could be found in the infarction zones of the G-CSF treatment group,while majority of the infiltrative inflammatory cells in control group were neutrophils and there was no infiltrative cells and myocytes which were CD34 + expression,2 weeks after administration of ISO,there were a plenty of scars in control group, but not in treatment group. Conclusion: Rat bone marrow stem cells are mobilized by G-CSF and dextran sulfate sodium salt, and migrate to the site of myocardial infarction, and differentiate to viable cardiomyocytes or vascular endotheliocytes.The heart function is remarkably improved by regeneration of myocytes,inhibition of fibroatrophy and protection of ischemic myocardial structure.