中文摘要：

目的观察心肌梗死后移植内皮祖细胞（EPCs）时的细胞自噬变化，探讨自噬维持移植细胞存活和纤维蛋白凝胶保护细胞的作用。方法通过结扎左冠状动脉的前降支建立大鼠心肌梗死模型后，在正常区、梗死边缘区和梗死区分别注射从人脐带血中分选的EPCs。2h后取注射处组织，作半薄切片，观察纤维蛋白凝胶承载的EPCs分布。定位后作超薄切片，透射电镜下观察EPCs的自噬结构变化以及纤维蛋白凝胶与EPCs和心肌的相容性。结果与正常区相比，梗死边缘区发生自噬的EPCs增多，细胞内自噬结构也增多。梗死区的移植细胞的自噬显著增强，有的细胞坏死或凋亡。纤维蛋白凝胶与移植细胞和心肌的相容性良好，移植的EPCs在纤维蛋白凝胶中充分伸展，有的EPCs与心肌细胞黏附。结论在梗死边缘区移植EPCs后，轻度缺血刺激细胞发生自噬，这有利于维持移植细胞存活。纤维蛋白凝胶承载EPCs可避免细胞丢失和促进存活。

英文摘要：

Objective To investigate autophagic changes endothelial progenitor cells （EPCs） carried with fibrin glue after transplantation into the infarcted myocardial and to explore effects of autophagy on maintaining the implanted cells to survive and fibrin on protecting the cells. Methods The model of myocardial infarction was established with ligating the anterior descending branch of the left coronary artery of rats. The EPCs sorted from human umbilical cord blood were injected into the myocardium at the normal region, periphery of the infarcted region and infarcted region. After transplantation for two hours, the tissues at injection sites were removed, the semithin sections were prepared. Distribution of the EPCs carried with fibrin glue were examined. After positioning the implanted cells, the ultrathin sections were prepared. The changes of the autophagic structures in EPCs and compatibility of fibrin with EPCs and myocardium were evaluated. Results Compared with the normal region, the autophagic EPCs in the periphery of the infarcted region increased, and the autophagic structures in the cells increased. In the infarcted region, EPC autophagy enhanced significantly, and necrosis or apoptosis occurred in some cells. Compatibility of fibrin with EPCs and myocardium was good. The implanted cells in fibrin glue extended well, some EPCs adhered to cardiaomyocytes. Conclusion When EPCs are transplanted into the periphery of the infarcted region, mild ischemia induces autophagy of the cells, which is beneficial for maintaining survival of the transplanted cells. Carrying EPCs with fibrin glue may avoid of cell lose and promote cell survival.