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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24 h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。
Objective To investigate the effect of granulocyte colony-stimulating factor (G-CSF) on mobilization of autologous bone marrow stem cells in rats for cardiac function and its possible mechanism. Methods The rat model of myocardial infarction was induced by isoproterenol (ISO). The bone marrow stem cells mobilized G-CSF was used to mobilize autologous bone marrow stem cells to release and migrate to myocardial infarction. The rats were sacrificed 24 h and 48 h after ISO, At 4 weeks after ISO, MPA-V multi-channel physiology was used to detect the hemodynamics and cardiac function of rats, then the rats were sacrificed and the hearts were removed and observed by immunohistochemistry, HE staining and VG staining Infiltration of CD34 + cells and myocardial regeneration and myocardial fibrosis in rat heart. Results 4 weeks after ISO, hemodynamic parameters and cardiac function parameters of G-CSF mobilization group were improved than those of control group. At 24 h after ISO, CD34 + cells were infiltrated in the myocardial infarction area of the mobilized group, and CD34 + positive neonatal cardiomyocytes grew. After 4 weeks, scar tissue was less, myocardial fibrosis was mild, and myocardial basic structure was protected. Conclusions After acute myocardial infarction, G-CSF can mobilize autologous bone marrow stem cells to migrate, survive and differentiate into cardiomyocytes and vascular endothelial cells in myocardial infarction. By myocardial regeneration, the inhibition of ischemic myocardial fibrosis and protection of ischemia The basic structure of myocardium, while improving heart function.