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The Anti-apoptotic Mechanism of Metformin Against Apoptosis Induced by Ionizing Radiation in Human Peripheral Blood

S Kolivand, E Motevaseli, M Cheki

    Klinicka Onkologie : Casopis Ceske a Slovenske Onkologicke Spolecnosti
    |October 15, 2017
    PubMed
    Abstract

    Insights

    Metformin (MET) protects human blood cells from radiation-induced apoptosis by modulating BAX, CASP3, and BCL2 gene and protein expression. This study clarifies MET's anti-apoptotic mechanism against ionizing radiation.

    Area of Science:

    • Cell Biology
    • Radiation Oncology
    • Pharmacology

    Background:

    • Metformin (MET) previously demonstrated a role in reducing ionizing radiation (IR)-induced apoptosis in human peripheral blood mononuclear cells.
    • The precise anti-apoptotic mechanism of MET against IR exposure remained unclear.
    • This study investigated MET's mechanism in mitigating X-ray induced apoptosis in human peripheral blood mononuclear cells.

    Purpose of the Study:

    • To elucidate the molecular mechanism by which metformin protects human peripheral blood mononuclear cells from ionizing radiation-induced apoptosis.
    • To analyze the effects of metformin on the expression of key apoptosis-related genes (BAX, CASP3, BCL2) and proteins following X-ray irradiation.

    Main Methods:

    • Human peripheral blood mononuclear cells were pretreated with metformin and subsequently exposed to X-ray irradiation.
    • Gene expression levels of BAX, CASP3, and BCL2 were quantified using real-time quantitative polymerase chain reaction (qPCR).
    • Protein levels of BAX, CASP3, and BCL2 were assessed via Western blotting.

    Main Results:

    • Ionizing radiation increased BAX and CASP3 gene expression while decreasing BCL2 expression.
    • Metformin pretreatment reversed these changes, increasing BCL2 and decreasing BAX and CASP3 gene expression, and reducing the BAX/BCL2 ratio.
    • Metformin also reversed radiation-induced alterations in BAX, CASP3, and BCL2 protein levels.

    Conclusions:

    • Metformin protects mononuclear cells from ionizing radiation-induced apoptosis.
    • This protection is mediated through the induction of cellular anti-apoptotic signaling pathways.
    • Metformin's effects involve the modulation of BAX, CASP3, and BCL2 gene and protein expression.

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