| Background：Dying myocardial cells only can be saved at a certain extent, but necroticmyocardial can not be repaired effectively in acute myocardial infarction by currenttherapy method. Stem cell transplantation in the treatment of myocardial infarctionand other cardiovascular diseases has been demonstrated its unique.Especially,with itssuperiority of rich sources,convenient collection,no immune rejection whileself-transplantation and great proliferation ability in vitro, ADMSCs become the idealseed cells. However, a few studies has been performed on the treatment of myocardialinfarction by ADMSCs transplantation. It is important to explore the mechanisms ofthe treatment on myocardial infarction by ADMSCs transplantation.Objective：(1) To build the methods of separate and amplification HADMSCs with nodifferentiation in vitro.(2) To confirm that HADMSCs can survive and differentiate into cardiomyocyte–like cells in acute myocardial infarction model.(3) To explore the influences on cardiac function and the possible mechanismsof therapying myocardial infarction in rats after HADMSC transplanted intopost-infarct myocardium.Methods：(1) Abdominal adipose tissues were obtained from healthy young individualsand separated with collagenase digestion and attachment culture methods. AndHADMSC were cultured in vitro for its passaged.Surface molecular and cell cycleidentification were detected of the3rd generation HADMSCs. The3rd generationHADMSCs were labelled with Brdu and then observed under a fluorescencemicroscope.(2)Thirty rats were divided into three groups randomly：sham operation withPBS injection(sham group,n=10)，acute myocardial infarction model with PBS injection(control group,n=10) and acute myocardial infarction model withHADMSCs transplantation (HADMSCs group,n=10). Acute myocardial infarctionrats were established by ligating of the left anterior descending artery, and infarctionmodels were confirmed by ECG. HADMSCs labelled by Brdu were injected into thecenter and the border of the MI area one week after AMI．The same volume of PBSwas injected into the MI area of the control group and sham group．(3) Echocardiography was performed to evaluate the cardiac function beforeoperation,1week and5weeks after AMI. The hearts were harvested5weeks afterAMI. Infarcted myocardium tissue was made into paraffin section and sectioned forHE stain. The percentage of left ventricular infarct size was calculated by theImageTool3.0pathological image analysis system. The expression of Brdu and cTnIwere observed to confirm the presence and differentiation of labelled cells byimmunohistochemistry.Results：(1) HADMSCs could be isolated and cultured with no differentiation in vitro forcontinuous culture of10th generation. The expression of CD44and CD29werepositive in these cells，but CD117and CD45were negative．(2) The value of LVDd、LVSd and EF were not significantly different with theHADMSCs group1weeks after AMI,compared with control group．Compared withsham group，the value of LVDd and LVSd were higher but EF was lower inHADMSCs group and AMI control group1weeks after AMI（p<0.05）.Comparedwith AMI control group，the value of LVDd and LVSd were lower but EF washigher in HADMSCs group5weeks after AMI（p<0.05）.(3) The myocardial tissue HE staining showed that infarction was visible in bothHADMSCs group and the AMI control group.5weeks after AMI，compared withcontrol group，the percentage of left ventricular infarct size was less than that inHADMSCs group（p<0.05）.(4) The positive expression of Brdu and cTnI were showed in HADMSCs groupby immunohistochemistry.Conclusion：(1) The experiment proves that HADMSCs can be isolated and cultured and amplificated with no differentiation in vitro successfully.(2)Transplantation HADMSCs after AMI can survive and differentiate intocardiomyocyte-like cells result in reducing the infarct size and improving the heartfunction. |
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