ABSTRACT
BACKGROUND:Myocardial infarction leads to ischemic changes in the myocardium, triggering the emergence of ventricular remodeling, which is an important cause of death. Myocardial infarction is a common disease in the middle-aged and elderly population, but autologous bone marrow mesenchymal stem cells from these patients exhibit a weak ability of proliferation and differentiation. Therefore, a positive attempt of allogeneic stem cel transplantation is required in order to obtain better therapeutic outcomes. OBJECTIVE:To explore the effect of al ogeneic bone marrow mesenchymal stem cel s on ventricular remodeling after myocardial infarction. METHODS:Bone marrow mesenchymal stem cel s from 10 neonatal rats and 10 adult rats were isolated, cultured and identified. Another 40 rats were randomly assigned into four groups (n=10/group):model group, neonatal rat cel transplantation group, adult rat cel transplantation group, or sham group. Animal models of myocardial infarction were made in rats in the al groups except for the sham group in which the rats were given sham operation. Rats in the two cel transplantation groups were given the corresponding cel transplantation. Four weeks postoperatively, heart function of rats was detected in each group, and cardiac tissues were taken to detect changes in col agen formation and blood vessel density in the infarct area. RESULTS AND CONCLUSION:Four weeks after surgery, rats in the model group showed significant changes in cardiac function indexes as compared with the other groups (P0.05). Meanwhile, compared with the model group, significantly decreased collagen formation and increased blood vessel density were found in both two cell transplantation groups (P<0.05). Additionally, the vascular density of the infarct area was highest in the sham group (P<0.05). Experimental results show that both neonatal and adult rat bone marrow mesenchymal stem cel transplantation can improve cardiac function of rats, reduce the formation of collagen in the infarct area and delay ventricular remodeling after myocardial infarction.