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Background <p>Doxorubicin (Dox) is a chemotherapy medication used in the therapy of cancers. However, despite its killing of cancer cells, Dox is toxic to the heart and can lead to heart failure. This outcome in turn poses a therapeutic challenge given the limited treatment options available to these individuals.</p> Objectives <p>This study examines how CeO₂ nanoparticles, through oxidative stress, inflammation, apoptosis, and mitochondrial function, reduced Dox toxicity in human cardiac myocyte (HCM) cells.</p> Methods <p>Following detection of the optimal doses of CeO₂ nanoparticles using the MTT assay, HCM cells were treated with Dox (8.25 µM) and CeO₂ nanoparticles for 24&#xa0;h. Then, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) and the activity of superoxide dismutase (SOD) were determined. Furthermore, the mitochondrial membrane potential, mitochondrial swelling, and mitochondrial cytochrome c release were analyzed. The level of gene expression of IL-1β, IL-6, and TNF-α, as well as apoptosis, was also examined.</p> Results <p>The data of this work demonstrated that Dox significantly elevated levels of ROS and MDA and reduced GSH level and SOD activity, which is modified by CeO₂ nanoparticles. Also, Dox meaningfully increased inflammation markers and apoptosis and induced mitochondrial malfunction, which were meaningfully reduced by CeO₂ nanoparticles in a dose-response manner in HCM cells.</p> Conclusion <p>According to the present study results, CeO₂ nanoparticles, through a reduction in oxidative stress, inflammation, apoptosis, and mitochondrial malfunction, can have therapeutic potential in HCM cells toxicity induced by Dox.</p> Graphical Abstract <p></p>

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In vitro evaluation of CeO2 nanoparticles on doxorubicin induced cardiotoxicity: focused on oxidative stress, inflammation, apoptosis, and mitochondrial function

  • 期刊论文

  • 发表日期：

    2025年9月3日

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  • Fahad Alsaikhan

摘要

Background

Doxorubicin (Dox) is a chemotherapy medication used in the therapy of cancers. However, despite its killing of cancer cells, Dox is toxic to the heart and can lead to heart failure. This outcome in turn poses a therapeutic challenge given the limited treatment options available to these individuals.

Objectives

This study examines how CeO₂ nanoparticles, through oxidative stress, inflammation, apoptosis, and mitochondrial function, reduced Dox toxicity in human cardiac myocyte (HCM) cells.

Methods

Following detection of the optimal doses of CeO₂ nanoparticles using the MTT assay, HCM cells were treated with Dox (8.25 µM) and CeO₂ nanoparticles for 24 h. Then, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) and the activity of superoxide dismutase (SOD) were determined. Furthermore, the mitochondrial membrane potential, mitochondrial swelling, and mitochondrial cytochrome c release were analyzed. The level of gene expression of IL-1β, IL-6, and TNF-α, as well as apoptosis, was also examined.

Results

The data of this work demonstrated that Dox significantly elevated levels of ROS and MDA and reduced GSH level and SOD activity, which is modified by CeO₂ nanoparticles. Also, Dox meaningfully increased inflammation markers and apoptosis and induced mitochondrial malfunction, which were meaningfully reduced by CeO₂ nanoparticles in a dose-response manner in HCM cells.

Conclusion

According to the present study results, CeO₂ nanoparticles, through a reduction in oxidative stress, inflammation, apoptosis, and mitochondrial malfunction, can have therapeutic potential in HCM cells toxicity induced by Dox.

Graphical Abstract