Thyroid hormones improve cardiac function and decrease expression of pro-apoptotic proteins in the heart of rats 14...

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.