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Background <p>Myocardial ischemia/reperfusion injury (MI/RI) is a pressing clinical concern that necessitates the development of innovative therapeutic strategies, particularly those based on natural compounds. Dysregulated iron metabolism and excessive reactive oxygen species (ROS) production have been extensively implicated in exacerbating MI/RI. Effective therapeutic approaches targeting both iron metabolism and ROS may offer a promising avenue for reducing MI/RI-induced cellular damage.</p> Objective <p>This study aimed to evaluate the protective effects of Obacunone (OB) on oxygen and glucose deprivation/reperfusion (OGD/R)-induced injury in H9c2 cardiomyoblast cells and elucidate its underlying mechanisms of action.</p> Results <p>Treatment with OB significantly improved cell viability and reduced apoptosis in H9c2 cells subjected to OGD/R. OB also alleviated oxidative stress by decreasing intracellular ROS levels and iron accumulation while preventing glutathione depletion. Furthermore, OB activated the Nrf2 signaling pathway, resulting in the upregulation of SLC7A11 and GPX4, two key mediators of ferroptosis inhibition.</p> Conclusion <p>OB exerts a protective effect against OGD/R-induced injury in H9c2 cells by inhibiting ferroptosis through the activation of the Nrf2/SLC7A11/GPX4 axis, suggesting its potential as a therapeutic agent for mitigating MI/RI.</p> Graphical abstract <p></p>

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Obacuone improves oxygen–glucose deprivation/reoxygenation-induced H9c2 cell damage by inhibiting ferroptosis

  • 期刊论文

  • 发表日期：

    2025年2月13日

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  • Ling Gao,
  • Jianhai Chen

摘要

Background

Myocardial ischemia/reperfusion injury (MI/RI) is a pressing clinical concern that necessitates the development of innovative therapeutic strategies, particularly those based on natural compounds. Dysregulated iron metabolism and excessive reactive oxygen species (ROS) production have been extensively implicated in exacerbating MI/RI. Effective therapeutic approaches targeting both iron metabolism and ROS may offer a promising avenue for reducing MI/RI-induced cellular damage.

Objective

This study aimed to evaluate the protective effects of Obacunone (OB) on oxygen and glucose deprivation/reperfusion (OGD/R)-induced injury in H9c2 cardiomyoblast cells and elucidate its underlying mechanisms of action.

Results

Treatment with OB significantly improved cell viability and reduced apoptosis in H9c2 cells subjected to OGD/R. OB also alleviated oxidative stress by decreasing intracellular ROS levels and iron accumulation while preventing glutathione depletion. Furthermore, OB activated the Nrf2 signaling pathway, resulting in the upregulation of SLC7A11 and GPX4, two key mediators of ferroptosis inhibition.

Conclusion

OB exerts a protective effect against OGD/R-induced injury in H9c2 cells by inhibiting ferroptosis through the activation of the Nrf2/SLC7A11/GPX4 axis, suggesting its potential as a therapeutic agent for mitigating MI/RI.

Graphical abstract