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Related Experiment Video

Updated: Apr 7, 2026

A Murine Model of Myocardial Ischemia-reperfusion Injury through Ligation of the Left Anterior Descending Artery
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T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of

Alexandre Luz de Castro1, Angela Vicente Tavares1, Rafael Oliveira Fernandes1

  • 1Laboratório de Fisiologia Cardiovascular, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite 500, sala 01, Porto Alegre, RS, CEP 90050170, Brazil.

Molecular and Cellular Biochemistry
|July 11, 2015
PubMed
Summary

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Thyroid hormone (TH) administration improved nitric oxide (NO) bioavailability and endothelial nitric oxide synthase (eNOS) expression in rats after myocardial infarction, mitigating harmful reactive oxygen species (ROS) levels.

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Molecular Biology

Background:

  • Myocardial infarction (MI) reduces nitric oxide (NO) bioavailability and increases reactive oxygen species (ROS), harming the heart.
  • Thyroid hormone (TH) administration shows promise in mitigating ischemic injury effects.
  • Understanding TH's impact on NO pathways post-MI is crucial for therapeutic strategies.

Purpose of the Study:

  • To investigate the effect of TH on NO bioavailability after myocardial infarction.
  • To assess the impact of TH on endothelial nitric oxide synthase (eNOS) expression in infarcted hearts.
  • To evaluate TH's influence on oxidative stress markers post-MI.

Main Methods:

  • Male Wistar rats were divided into Sham-operated (SHAM), myocardial infarction (AMI), and infarcted + TH (AMIT) groups.
Keywords:
Heart failureNitric oxideOxidative stressThyroid hormones

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  • The AMIT group received T3 and T4 (2 and 8 µg/100 g/day) for 26 days; controls received saline.
  • Echocardiography, biochemical, and molecular analyses of left ventricle tissue were performed.

    • Main Results:

    • AMI rats exhibited a 38% increase in ROS levels, which TH administration prevented in AMIT rats.
    • TH administration significantly increased eNOS expression, nitric oxide synthase (NOS) activity, and nitrite levels in AMIT rats.
    • Thyroid hormone treatment also led to increased PGC-1α expression in the infarcted heart.

    Conclusions:

    • Thyroid hormone administration positively modulates eNOS expression and NO bioavailability in the context of myocardial infarction.
    • TH treatment offers a potential therapeutic approach to counteract the detrimental effects of ischemia-reperfusion injury.
    • These findings highlight TH's role in preserving cardiac function through improved NO signaling pathways.