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Updated: Mar 28, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Thyroid hormones improve cardiac function and decrease expression of pro-apoptotic proteins in the heart of rats 14
Alexandre Luz de Castro1, Rafael Oliveira Fernandes1, Vanessa D Ortiz1
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.
Insights
Thyroid hormones (TH) protect against cardiac remodeling post-myocardial infarction by reducing apoptosis. This study shows TH treatment improved heart function and decreased pro-apoptotic proteins in infarcted rats.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Apoptosis plays a critical role in pathological cardiac remodeling following myocardial infarction (MI).
- Thyroid hormones (TH) have demonstrated potential anti-apoptotic effects in previous research.
- Understanding TH's impact on apoptosis-related proteins is crucial for developing new therapeutic strategies for post-MI recovery.
Purpose of the Study:
- To investigate the effects of thyroid hormones (TH) on the expression of apoptosis-associated proteins in rat hearts 14 days after myocardial infarction.
- To evaluate the impact of TH administration on cardiac function and ventricular wall thickness in an experimental model of myocardial infarction.
Main Methods:
- Male Wistar rats were divided into four groups: Sham-operated (SHAM), myocardial infarction (AMI), SHAM + TH, and AMI + TH.
- Animals received T3 and T4 hormones daily via gavage for 12 days.
- Cardiac function was assessed using hemodynamic and echocardiographic analyses, followed by molecular analysis of heart tissue to determine protein expression levels.
Main Results:
- TH administration preserved ventricular wall thickness and improved cardiac function in infarcted rats.
- Myocardial infarction led to increased levels of pro-apoptotic proteins p53 and JNK, which were prevented by TH treatment.
- TH administration reduced the Bax:Bcl-2 ratio, indicating a shift towards reduced apoptosis.
Conclusions:
- Thyroid hormones effectively improve cardiac function and reduce apoptosis-related protein expression 14 days after myocardial infarction.
- TH treatment mitigates cardiac remodeling by inhibiting key pro-apoptotic pathways.
- These findings suggest TH could be a potential therapeutic agent for managing post-myocardial infarction cardiac dysfunction.
Abstract:
Apoptosis is a key process associated with pathological cardiac remodelling in early-phase post-myocardial infarction. In this context, several studies have demonstrated an anti-apoptotic effect of thyroid hormones (TH). The aim of this study was to evaluate the effects of TH on the expression of proteins associated with the apoptotic process 14 days after infarction. Male Wistar rats (300-350 g) (n = 8/group) were divided into four groups: Sham-operated (SHAM), infarcted (AMI), sham-operated + TH (SHAMT) and infarcted + TH (AMIT). For 12 days, the animals received T3 and T4 [2 and 8 µg/(100 g day)] by gavage. After this, the rats were submitted to haemodynamic and echocardiographic analysis, and then were sacrificed and the heart tissue was collected for molecular analysis. Statistical analyses included two-way ANOVA with Student-Newman-Keuls post test. Ethics Committee number: 23262. TH administration prevented the loss of ventricular wall thickness and improved cardiac function in the infarcted rats 14 days after the injury. AMI rats presented an increase in the pro-apoptotic proteins p53 and JNK. The hormonal treatment prevented this increase in AMIT rats. In addition, TH administration decreased the Bax:Bcl-2 ratio in the infarcted rats. TH administration improved cardiac functional parameters, and decreased the expression of pro-apoptotic proteins 14 days after myocardial infarction.
