Introduction:
Systemic inflammatory and immune suppressive incidents constitute a significant hallmark of red blood cell transfusion's adverse effects. These adverse side effects are seemingly associated with old blood transfusion; therefore, we aim to investigate the underlying mechanism of fresh autologous blood transfusion (fABT) and its subsequent effect in diabetic mice.

Material and methods:
In the present study, we utilized 60 Swiss male mice aged 6-8 weeks, categorized into 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 analysis, 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:
Results showed that fresh autologous blood transfusion markedly reduced M2 macrophage polarization, enhanced hepatic mitochondrial metabolism, reduced hepatic oxidative stress, and promoted red blood cells' oxygen-carrying capacity while reducing its osmotic fragility and oxygen consumption. Moreover, we found that fABT promoted the IGF2/PI3K signaling pathway, These results indicate the vital necessity of providing fresh autologous blood transfusion during therapy or surgeries.

Conclusions:
In conclusion, our results are the first to highlight the underlying mechanism in which how fABT modulates physiological patterns in diabetic animals model, proposing a sound basis for utilizing fABT in clinical applications.