Effect of intravenous transplantation of hUCB-MSCs on M1/M2 subtype conversion in monocyte/macrophages of AMI mice

Abstract

BackgroundThe transplantation of stem cells is effective in the treatment of acute myocardial infarction (AMI). But the mechanisms of stem cell transplantation for the treatment of AMI have not been clearly confirmed. This article is to compare cardiac function, myocardial fibrosis, inflammatory cell infiltration, apoptotic index, and M1 macrophage to M2 macrophage ratios 4 weeks after hUCB-MSCs transplantation in Mice with AMI. MethodsMice model of AMI was divided into two groups randomly. Human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) were transplanted to the intervention group via mice tail vein, and saline solution was used for the control group. Masson staining calculated the proportion of the remaining myocardium and collagen volume fraction (CVF) in the infarct area, flow cytometry and immunofluorescence staining to analyze M1 / M2 subtype and its ratio were performed. Serum IL-6 and galectin-3 levels were determined using ELISA. ResultsThe results showed that heart function of the intervention group was significantly better than that of the control group, and the degree of fibrosis and inflammation in the intervention group were lower than those in the control group. The ratio of monocyte M1/M2 in peripheral blood, spleen and myocardial tissue in hUCB-MSCs transplantation was significantly lower than that of the control group. But there is no significant difference in the apoptotic index between two groups. The ELISA results showed that serum IL-6 (97.98 ± 5.94 pg/ml) and galectin-3 levels (69.94 ± 5.11 ng/ml) were lower in the intervention group than in the control group (IL-6: 118.2 ± 5.03 pg/ml; galectin-3: 83.14 ± 2.76 ng / ml). However, compared with the control group, only IL-6 showed a significant decrease in the intervention group (p = 0.032). ConclusionIntravenous transplantation of hUCB-MSCs can reduce inflammatory response by stimulating the conversion of intracardiac and extracardiac macrophage subtype M1 / M2, decrease the serum IL-6 and galectin-3 levels, improve cardiac function and protect the infarcted myocardium.