Abstract
INTRODUCTION: Systemic inflammatory and immunosuppressive incidents constitute a significant hallmark of the adverse effects of RBC transfusion on red blood cells. These adverse side effects are seemingly associated with old blood transfusions; therefore, we aimed to investigate the underlying mechanism of fresh autologous blood transfusion (fABT) and its subsequent effect in diabetic mice. MATERIAL AND METHODS: In the present in vivo study, we utilized 60 Swiss male mice aged 6-8 weeks, categorized as normal, diabetic, and freshly transfused with autologous blood. After treating the mice accordingly, further experimentations took place as we assessed the M1/M2 macrophage polarization concerning CD16/CD32/CD206 cells by flow cytometry, determined the mitochondrial metabolism using Lowry's method, measured hepatic oxidative stress using MDA and SOD assays, and examined the erythrocytic oxygen-carrying capacity (Q value) and oxygen consumption rate (OCR) and osmotic fragility. RESULTS: The results showed that fresh autologous blood transfusion markedly reduced M2 macrophage polarization, enhanced hepatic mitochondrial metabolism, reduced hepatic oxidative stress, and promoted the oxygen-carrying capacity of red blood cells while reducing osmotic fragility and oxygen consumption. Moreover, we found that fABT promoted the IGF2/PI3K signaling pathway, indicating the vital necessity of providing fresh autologous blood transfusion during therapy or surgery. CONCLUSIONS: Our results are the first to highlight the underlying mechanism by which fABT modulates physiological patterns in a diabetic animal model, and provide a sound basis for utilizing fABT in clinical applications.