Objective To investigate the effect and mechanism of umbilical cord blood mononuclear cells on angiogenesis in rats with acute myocardial infarction.
Methods HCMNCs were isolated and labeled with BrdU. A rat model of acute myocardial infarction was established in 25 rats by coronary artery ligation. Twenty rats were randomly divided into myocardial infarction group and HCMNCs group, 10 in each group, and the other 10 as sham. surgical group. After successful modeling, HCMNCs were injected around the myocardial infarction in the HCMNCs group, and L-DMEM medium was injected into the same site in the sham-operated group and the model group. Four weeks after transplantation, echocardiography was used to detect cardiac function, HE staining was used to observe myocardial pathological changes, BrdU staining was used to detect the survival of transplanted cells, and immunohistochemical staining was used to detect myocardial infarction edge microvessel density (MVD), CD31, vascular endothelial growth factor (VEGF). ) protein expression, and Western blot was used to detect the protein levels of CD31 and VEGF in myocardial tissue.
Results Compared with the sham operation group, the levels of left ventricular end-systolic diameter (LVEDs), left ventricular end-diastolic diameter (LVEDd), left ventricular ejection fraction (LVEF), left ventricular short-axis shortening rate ( Compared with the myocardial infarction group, the levels of LVEDs and LVEDd in the 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-operated group was normal, and the myocardial cells in the myocardial infarction group were disordered and infiltrated with a large number of inflammatory cells; the structure of myocardial cells in the HCMNCs group was basically normal. BrdU staining showed that BrdU-labeled positive cells were not detected in both the sham-operated group and the myocardial infarction group, while scattered BrdU-positive cells were found in the infarcted area of the HCMNCs group, which were involved in the composition of the vessel wall. Compared with the sham operation group, the CD31 and VEGF protein optical density, protein relative expression and MVD in the myocardial infarction group and HCMNCs group decreased (P<0.05). And the 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 cardiac function.