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May 28, 2026Advances in Pharmacological and Pharmaceutical SciencesOpen Access

Nrf2/GPX4‐Dependent Ferroptosis Inhibition: The Central Mechanism Underpinning Germacrone‐Induced Cardioprotection in Myocardial Infarction

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Authors

JLJ LiaoZWZitian WangZHZhou Huang

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Overview

Randomized trial evaluates germacrone's cardioprotective effects via ferroptosis inhibition in myocardial infarction, suggesting new treatment avenues.

Key Points

  • This research aims to explore how germacrone inhibits ferroptosis to protect against myocardial infarction.
  • Utilized a murine model of ISO-induced myocardial infarction and an in vitro injured H9c2 cardiomyocyte model.
  • Administered germacrone at doses of 25, 50, and 100 mg/kg for 7 consecutive days to the experimental group.
  • Measured myocardial injury markers and analyzed the effects of Nrf2/GPX4 axis modulation using ML385, a specific Nrf2 inhibitor.
  • Germacrone significantly decreased myocardial injury and improved cardiac function in mice post-ISO administration.
  • The treatment lowered levels of myocardial injury and inflammatory markers across all experimental models.
  • Germacrone reduced apoptotic rates in H9c2 cells and inhibited ferroptosis by upregulating Nrf2, GPX4, and HO-1 proteins.

Cite This Study

Liao et al. (2026) studied this question.

synapsesocial.com/papers/6a17dcdf3fad632b0f9d9965https://doi.org/10.1155/adpp/7893262
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