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目的观察骨髓间充质干细胞(MSCs)经静脉途径移植对阿霉素诱导的扩张型心肌病(DCM)大鼠心功能的影响。方法建立大鼠阿霉素性心肌病模型,随机分为三组:DCM空白组(B组)、静脉移植组(C组)和静脉对照组(D组),另设正常对照组(A组)。经尾静脉注射在体外扩增并DAPI标记的骨髓间充质干细胞和培养基至C组和D组大鼠,A组和B组大鼠不干预。移植后8周心脏彩超观察左室舒张末径(LVDD)、左室射血分数(LVEF),多导生理记录仪观察左室最大压力上升速率(+LVdp/dtmax)、左室最大压力下降速率(-LVdp/dtmax),并分析组织病理学特征。结果细胞移植后8周,C组LVEF高于B组和D组;LVDD稍低于B组和D组;+LVdp/dtmax明显高于B组,也显著高于D组;-LVdp/dtmax明显高于B组和D组;C组心肌中可见带有蓝色荧光的DAPI标记的骨髓MSCs,心肌胶原容积百分比低于B组和D组,毛细血管计数高于B组和D组;C组VEGF水平明显高于B组和D组。结论骨髓MSCs静脉移植治疗阿霉素诱导的扩张型心肌病大鼠,提高VEGF水平,促进心肌毛细血管新生,减少胶原纤维,改善心功能。
Objective To observe the effects of bone marrow mesenchymal stem cells (MSCs) transplantation on the cardiac function of doxorubicin-induced dilated cardiomyopathy (DCM) rats. Methods A rat model of adriamycin-induced cardiomyopathy was established and randomly divided into three groups: DCM blank group (group B), vein graft group (group C) and vein control group (group D) ). Rats in groups A and B were not intervened by tail vein injection of DAPI-labeled bone marrow mesenchymal stem cells and culture medium to groups C and D in vitro. Left ventricular end-diastolic diameter (LVDD), left ventricular ejection fraction (LVEF) and maximum pressure rise rate (+ LVdp / dtmax) were observed by echocardiography 8 weeks after transplantation. (-LVdp / dtmax), and analyzed histopathological features. Results After 8 weeks of cell transplantation, LVEF in group C was significantly higher than that in group B and group D; LVDD was slightly lower than group B and group D; LVdp / dtmax was significantly higher than group B and significantly higher than group D Which was higher than those in group B and group D. The DAPI-labeled bone marrow MSCs with blue fluorescence were observed in group C, the percentage of myocardial collagen volume was lower than group B and group D, and the capillary count was higher than group B and group D. Group C VEGF levels were significantly higher than the B and D groups. Conclusion The bone marrow MSCs were transplanted intravenously in doxorubicin-induced dilated cardiomyopathy rats to increase the level of VEGF, promote myocardial capillary angiogenesis, reduce collagen fibers and improve cardiac function.