Mechanisms of Action of Umbilical Cord Mesenchymal Stem Cells in Type 2 Diabetes Mellitus Treatment

Type 2 diabetes mellitus affects the quality of life of patients significantly. Traditional treatments have certain limitations; however, cellular therapy has demonstrated remarkable positive effects, such as improved blood glucose and lipid levels, repaired pancreatic and renal structure, and improvements in diabetic complications. A type 2 diabetes mellitus rat model was constructed, and rats were divided into six groups. Four groups were further formed to evaluate the antiinflammatory effects of umbilical cord mesenchymal stem cells. The antiinflammatory effects of human umbilical cord mesenchymal stem cells were demonstrated using inflammatory factors and M2 macrophages, a type of antiinflammatory macrophage. Western blotting and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining were performed to further elaborate the mechanism of action of human umbilical cord mesenchymal stem cells in type 2 diabetes mellitus treatment. We confirmed that human umbilical cord mesenchymal stem cells could efficiently treat type 2 diabetes mellitus. We conducted an ameliorative fasting blood glucose test and an oral glucose tolerance test and assessed the recovery of liver and renal function using biochemical factors (such as TC, TG, BUN, and Ccr, among others). The antiinflammatory effect of the treatment was demonstrated by the increased expression of biomarkers in M2 macrophages and reduced secretion of inflammatory cytokines, such as TNF-α. The regulatory mechanism was involved in the TLR4/NF-κB signaling pathway. The apoptosis of pancreatic tissues in type 2 diabetes mellitus was also inhibited by umbilical cord mesenchymal stem cells, contributing to relief from type 2 diabetes mellitus symptoms. In conclusion, our findings confirmed that efficient type 2 diabetes mellitus treatment using human umbilical cord mesenchymal stem cells was related to antiinflammatory effects mediated via TLR4/NF-κB signaling inhibition and apoptosis attenuation in pancreatic tissues.