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Involvement of TRPM2 Channel on Doxorubicin-Induced Experimental Cardiotoxicity Model: Protective Role of Selenium

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A Correction to this article was published on 11 March 2023

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Abstract

Doxorubicin (DOXR) is an important chemotherapeutic drug used in cancer treatment for many years. Several studies reported that the use of DOXR increased toxicity by causing an increase in oxidative stress (OS), especially in the heart. In this study, we investigated the protective effect of selenium (Se) and the role of transient receptor potential melastatin‐2 (TRPM2) channel activation by using N-(p-amylcinnamoyl) anthranilic acid (ACA) in a model of DOXR-induced cardiotoxicity. Sixty female rats were equally divided into the control, dimethyl sulfoxide (DMSO), DOXR, DOXR + Se, DOXR + ACA, and DOXR + Se + ACA groups. Glutathione (GSH), glutathione peroxidase (GSH-Px), caspases (Cas) 3 and 9, interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α), reactive oxygen species (ROS), poly [ADP-ribose] polymerase 1 (PARP-1), and TRPM2 channel levels were measured by ELISA. In addition, histopathological examination was performed in cardiac tissues and TNF-α, caspase 3, and TRPM2 channel expression levels were determined immunohistochemically. The levels of GSH, GSH-Px, caspases 3 and 9, IL-1β, TNF-α, ROS, PARP-1, and TRPM2 channel in serum, and cardiac tissue in the DOXR group were higher than in the control and DMSO groups (p < 0.05). However, these parameters in Se and/or ACA treatment groups were lower than in the DOXR group (p < 0.05). Also, we determined that Se and/or ACA treatment together with DOXR application decreased the TNF-α, Cas-3, and TRPM2 channel expression levels in the cardiac tissue. The data showed that administration of Se and/or ACA treatment together with DOXR may be used as a therapeutic agent in preventing DOXR-induced cardiotoxicity.

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Data Availability

The data that support the findings of this study are available from the corresponding author upon request.

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Acknowledgements

This study was supported by Van Yuzuncu Yil University Scientific Research Projects (BAP) Coordinatorship with project numbered TYD-2021-9714.

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Authors and Affiliations

  1. Department of Biophysics, Faculty of Medicine, Van Yuzuncu Yil University, TR-65090, Van, Turkey

    Kenan Yıldızhan

  2. Department of Biochemistry, Faculty of Medicine, Van Yuzuncu Yil University, Van, Turkey

    Zübeyir Huyut

  3. Department of Histology and Embryology, Faculty of Medicine, Van Yuzuncu Yil University, Van, Turkey

    Fikret Altındağ

Authors
  1. Kenan Yıldızhan
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  2. Zübeyir Huyut
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  3. Fikret Altındağ
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Contributions

Study design: K.Y. Data collection: all authors. Statistical analysis: K.Y., Z.H., and F.A. Data interpretation: Z.H., K.Y., and F.A. Manuscript preparation: K.Y. and Z.H. Literature search: Z.H., K.Y., and F.A. All authors reviewed the manuscript.

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Correspondence to Kenan Yıldızhan.

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The original online version of this article was revised: Under the heading "Biochemical Measurement in Cardiac Homogenates and Serum" in the first line is should read "The levels of TRPM2 (MyBioSource, Cat#MBS9395911)".

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Yıldızhan, K., Huyut, Z. & Altındağ, F. Involvement of TRPM2 Channel on Doxorubicin-Induced Experimental Cardiotoxicity Model: Protective Role of Selenium. Biol Trace Elem Res 201, 2458–2469 (2023). https://doi.org/10.1007/s12011-022-03377-2

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