骨髓干细胞动员对心肌梗死大鼠心功能的影响

目的探讨应用粒细胞集落刺激因子(G-CSF)动员大鼠自体骨髓干细胞治疗心肌梗死,对心功能的影响及其可能机制.方法用异丙肾上腺素(ISO)制作大鼠心肌梗死模型,用骨髓干细胞动员剂G-CSF动员自体骨髓干细胞释放和迁移至心肌梗死灶,于用ISO后24,48 h杀死大鼠,取出心脏;用ISO后4周,先用MPA-V多导生理仪检测大鼠血流动力学、心功能指标,随后杀死大鼠,取出心脏,通过免疫组化、HE染色和VG染色方法观察大鼠心梗灶的CD34 细胞的浸润及心肌再生、心肌纤维化的情况.结果用ISO后4周,G-CSF动员组大鼠血流动力学指标、心功能参数均比对照组改善.用ISO后24h后,动员组大鼠心梗区可见CD34 细胞浸润,并有CD34 阳性的新生心肌细胞生长,4周后瘢痕组织少,心肌纤维化程度轻,心肌基本结构得到保护.结论急性心梗发生后,应用G-CSF能动员自体骨髓干细胞向心梗灶内迁移、存活和向心肌细胞、血管内皮细胞等分化;并通过心肌再生、抑制缺血心肌纤维化和保护缺血心肌基本结构,而改善心功能.

Influence of bone marrow stem cell mobilization on heart function in myocardial infarction rat

Objective: To investigate the influence of heart function and the possible mechanism of repairing myocardial infarction by mobilizing the bone marrow stem cell in rat. Methods: After injection of isoprenaline (ISO) interaperitoneally to develop acute ischemic model, rat bone marrow stem cells were mobilized by G-CSF and migrated to the site of myocardial infarction. Hearts were harvested after using ISO 24 and 48 hours; 4 weeks after administration of ISO for histopathological examination. Immunohistochemisty, HE and VG stain were used to detect infiltration of CD34 monocytes and the regeneration of myocytes and the inhibition of fibroatrophy of ischemic myocardium. 4 weeks after injection heart function of each group was measured using a MPA-V instrument. Results: Compared with the control group, heart function of the G-CSF mobilization group was improved. 24 hours after administration of ISO, a large amount of infiltrative monocytes and some regenerative myocytes with positive expression of CD34 were found in the infarct zones of the mobilization group. 4 weeks after administration of ISO, there were fewer scars in the mobilization group. Conclusions: Rat bone marrow stem cells are mobilized by G-CSF and migrated to the site of myocardial infarction, and differentiated into viable cardiomyocytes or vascular endothelial. The heart function is remarkably improved by regeneration of myocytes and inhibition of fibroatrophy and protection of ischemic myocardial structure.