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 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.

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.

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