Exploration of the mechanism of reinfusion of fresh autologous blood in type 2 diabetic body to induce macrophage polarization and inhibit erythrocyte damage

Type 2 diabetes (T2D) triggers an inflammatory response that can damage red blood cells. M2 macrophages have inhibitory effects on inflammation and play an important role in tissue damage repair and fibrosis. Autologous blood transfusion has the potential to inhibit red blood cell damage by mediating macrophage polarization. Swiss mice were used to establish a suitable type 2 diabetes model and autologous blood transfusion was performed. The mice were executed, the blood of the mice was collected, and CD14+ monocytes were sorted. The expression levels of phenotypic molecules CD16, CD32 and CD206 in CD14+ monocytes were analyzed by flow cytometry. The proportion of M1 and M2 macrophages were analyzed by flow cytometry. The Q value, P50, 2,3-DPG and Na+-K+-ATPase of red blood cells were detected. The red blood cell osmotic fragility test analyzed the RBC osmotic fragility. Western Blot analysis was used to analyze the expression changes of erythrocyte surface membrane proteins or transporters EPB41, S1P, GLTP and SPPL2A. Autologous blood transfusion induced a significant increase in the number of macrophages. The state and capacity of blood cells improved with autologous blood transfusion. Reinfusion of fresh autologous blood in T2D body made erythrocytes shrank. The expression of erythrocyte-related proteins proved that the erythrocyte injury in the Fresh+T2D group was significantly reduced. The reinfusion of fresh autologous blood into the body of patients with type 2 diabetes can induce macrophage polarization to M2, thereby inhibiting red blood cell damage.