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Updated: Jun 28, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
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Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

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Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in

Laís Lopes Gonçalves1, Ildernandes Vieira Alves1, Erika Ferreira Nicoli1

  • 1Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Brazil.

Journal of Cellular and Molecular Medicine
|June 27, 2026
PubMed
Summary

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Exercise training improves vascular reactivity in ovariectomized rats subjected to myocardial infarction.

PloS one·2019

Ellagic acid (EA) reduces cardiac fibrosis and ventricular dysfunction after myocardial infarction (MI) in ovariectomized rats. This cardioprotective effect is linked to EA's antioxidant and anti-inflammatory properties, improving nitric oxide (NO) bioavailability.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Oxidative Stress

Background:

  • Oestrogen deficiency exacerbates cardiac fibrosis post-myocardial infarction (MI) by increasing oxidative stress and decreasing nitric oxide (NO) bioavailability.
  • Myocardial infarction (MI) leads to significant cardiac remodeling, including fibrosis and ventricular dysfunction, particularly in the absence of oestrogen.

Purpose of the Study:

  • To investigate the cardioprotective effects of ellagic acid (EA), a natural antioxidant, against cardiac fibrosis in a rat model of MI with oestrogen deficiency.
  • To determine if EA attenuates post-MI cardiac fibrosis by modulating oxidative stress and pro-inflammatory pathways.

Main Methods:

  • Myocardial infarction (MI) was induced in ovariectomized rats via coronary artery ligation.
  • Ellagic acid (EA) was administered orally at 30 mg/kg for 4 weeks post-MI.
Keywords:
cardiac fibrosiscytokinesellagic acidnitric oxideovariectomyoxidative stress

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Last Updated: Jun 28, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
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Published on: March 7, 2022

  • Evaluated hemodynamic parameters, collagen deposition, infarct size, matrix metalloproteinase-8 (MMP-8), NO levels, superoxide anion, and inflammatory cytokines (IL-6).

    • Main Results:

    • MI induced ventricular dysfunction, increased cardiac collagen deposition, elevated MMP-8, IL-6, and superoxide anion levels.
    • EA treatment significantly improved hemodynamic function and reduced infarct size and collagen deposition.
    • EA administration enhanced NO bioavailability and decreased oxidative stress markers (superoxide anion) and inflammatory mediators (MMP-8, IL-6).

    Conclusions:

    • Ellagic acid (EA) effectively mitigates cardiac fibrosis and ventricular dysfunction following myocardial infarction (MI) in an oestrogen-deficient state.
    • EA exerts cardioprotection through potent antioxidant and anti-inflammatory mechanisms, including the enhancement of nitric oxide (NO) bioavailability.
    • Ellagic acid (EA) shows promise as a therapeutic agent for preventing cardiac complications in post-MI patients with oestrogen deficiency.