【Animal Modeling】-Umbilical cord blood mononuclear cells promote angiogenesis in rats with acute myocardial infarction and its mechanism

  Objective To investigate the effect and mechanism of cord blood mononuclear cells (HCMNCs) on angiogenesis in acute myocardial infarction (AMI) rats.

  Methods HCMNCs were isolated and labeled with BrdU. 25 rats were selected to establish an acute myocardial infarction rat model by coronary artery ligation. 20 rats were successfully modeled and randomly divided into myocardial infarction group and HCMNCs group, each with 10 rats, and the other 10 rats were taken as sham Surgery group. After successful modeling, the rats in the HCMNCs group were injected with HCMNCs around the myocardial infarction, and the sham operation group and the model group were injected with L-DMEM medium at the same site. Four weeks after transplantation, echocardiography was used to detect cardiac function, HE staining to observe myocardial pathological changes, BrdU staining to detect the survival of transplanted cells, and immunohistochemical staining to detect microvessel density (MVD), CD31, and vascular endothelial growth factor (VEGF) at the margin of myocardial infarction. ) Protein expression, Western blot method was used to detect CD31 and VEGF protein levels in myocardial tissue.

  Results Compared with the sham operation group, the levels of left ventricular end systolic diameter (LVEDs) and left ventricular end diastolic diameter (LVEDd) levels increased, left ventricular ejection fraction (LVEF), and left ventricular short axis shortening rate ( FS) level decreased (P<0.05); compared with myocardial infarction group, the levels of LVEDs and LVEDd in HCMNCs group decreased, while the levels of LVEF and FS increased (P<0.05). HE staining showed that the structure of myocardial cells in the sham operation group was normal, and the myocardial cells in the myocardial infarction group were arranged disorderly with a large amount of inflammatory cell infiltration; the structure of myocardial cells in the HCMNCs group was basically normal. BrdU staining showed that no BrdU-labeled positive cells were detected in the sham operation group and the myocardial infarction group. There were scattered BrdU-positive cells in the infarct area of the HCMNCs group, which participated in the composition of the blood vessel wall. Compared with the sham operation group, the CD31 and VEGF protein optical density values, relative protein expression and MVD of the myocardial infarction group and HCMNCs group were reduced (P<0.05); compared with the myocardial infarction group, the CD31 and VEGF protein optical density values of the HCMNCs group And relative protein expression and MVD increased (P<0.05).

  Conclusion HCMNCs can promote the establishment of collateral circulation in AMI rats, induce angiogenesis, and significantly improve ischemic heart function.