Related Experiment Video
Updated: Apr 7, 2026
A Murine Model of Myocardial Ischemia-reperfusion Injury through Ligation of the Left Anterior Descending Artery
Published on: April 10, 2014
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.
Unlabelled:
Myocardial infarction leads to a reduction in nitric oxide (NO) bioavailability and an increase in reactive oxygen species (ROS) levels. This scenario has been shown to be detrimental to the heart. Recent studies have shown that thyroid hormone (TH) administration presents positive effects after ischaemic injury. Based on this, the aim of this study was to evaluate the effect of TH on NO bioavailability as well as on endothelial nitric oxide synthase (eNOS) expression after myocardial infarction. Male Wistar rats were divided into three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted + TH (AMIT). During 26 days, the AMIT group received T3 and T4 (2 and 8 µg/100 g/day, respectively) by gavage, while SHAM and AMI rats received saline. After this, the rats underwent echocardiographic analysis were sacrificed, and the left ventricle was collected for biochemical and molecular analysis.
Statistical Analysis:
one-way ANOVA with Student-Newman-Keuls post test. AMI rats presented a 38% increase in ROS levels. TH administration prevented these alterations in AMIT rats. The AMIT group presented an increase in eNOS expression, in NOS activity and in nitrite levels. TH administration also increased PGC-1α expression in the AMIT group. In conclusion, TH effects seem to involve a modulation of eNOS expression and an improvement in NO bioavailability in the infarcted heart.
Insights
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.
- 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.
