| Background:Myocardial cells decrease after acute myocardial infarction (AMI), and mature cardiomyocytes have limited ability to regenerate. All these factors promote myocardial remodeling, resulting in cardiac decompensation and the development of heart failure. Current drug and reperfusion therapy can not reserve myocardial remodeling fundamentally, and can not be inhibit the subsequent development of heart failure. So the effect of treatment is not ideal. Although heart transplantation is a final selection of end-stage heart failure, fewer sources and immune rejection limit its clinical applications. Stem cells as an important aspect of regenerative medicine, they provides new hope for the treatment of heart failure after AMI because of their self-renewal, proloferation and differentiation capacity. Adipose-derived mesenchymal stem cells (ADSCs) have lots of advantages relative to other sources of mesenchymal stem cells, such as rich and available source, massively proliferated in vitro and no immune rejection and ethical issues. So it receives much concerns. Many mechanisms of ADSCs for the treatments have been proposed. Applying mesenchymal stem cells in the treatment of heart failure after AMI and exploring its therapeutic mechanism is still worthy of our attention and study. Objective:To research the effects of ADSCs on cardiac function after AMI in rats and preliminary explore its possible machanism for the treatments.Methods:1) Isolation, cultivation and identification of ADSCs. We get the fat of rats,separate and purify ADSCs. And we use flow cytometry to assess phenotypic identification and induce ADSCs to osteogenic and adipogenic defferentiation.2) ADSCs are transplated to the rats after AMI, to observe the therapeutic effects. SD rats are randomly divided four groups, and each one has eight rats. Group A, during the peocess of modeling, operative suture only crosses the vessel, with out ligation. Group B of AMI, after the models of AMI have operated, the rats give any treatment. Group C of L-DMEM, afte the models of AMI have operated, the rats are given200ul L-DMEM at the edge of myocardial infarction zone with aseptic miroinjector, the solution of L-DMEM is given at four points with50ul every one. Group D of ADSCs, afte the models of AMI have operated, the rats are given200ul cell suspension (number of cells with106/200ul) with the same method.7days and28days after the operation, all rats are given cardiac ultrasound. Afte28days, every one has hemodynamic test. Then all the hearts of the rats have TTC staining. Then praparation of frozen sections, the tissues have masson staining and immunofluorescense double staining (CD31as a marker of endothelial cells, FSP-1as a marker of fibroblast.Results:We isolate ADSCs successfully. CD29, CD90, CD105are positive expression, and CD31,CD45are negative expression. And ADSCs can be induced to osteogenic and adipogenic cells. The cardiac function of group A is superior to group B, C and D. cardiac function, hemodynamic of group D is improved significantly compared with group B and C. The area size of infartion and fibrosis is reduced in group D compared with group B,C. Double staining cells is observed, the number of group D is lower than group B.Conclusion:1.ADSCs can be isolated and cultivated successfully.2.ADSCs can improve cardiac function and remodeling of the rats after myocardiac infarction significantly. And it can reduce the degree of fibrosis which may be ralated to the inhibition of endothelial-mesenchymal transiton. |
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