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Thyroid hormones decrease the proinflammatory TLR4/NF-κβ pathway and improve functional parameters of the left

Alexandre Luz de Castro1, Rafael Oliveira Fernandes2, Vanessa D Ortiz2

  • 1Laboratory of Cardiovascular Physiology and Reactive Oxygen Species, Physiology Department, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Sarmento Leite Street, 500, CEP 90050-170, Porto Alegre, RS, Brazil; Centro Universitário Ritter dos Reis (Uniritter), Orfanotrófio Street, 555, CEP 90840-440, Porto Alegre, Rio Grande do Sul, Brazil.

Molecular and Cellular Endocrinology
|September 11, 2017
PubMed
Summary

Thyroid hormones (TH) reduce inflammation and oxidative stress in hearts after myocardial infarction. This anti-inflammatory action improves cardiac function, highlighting TH

Keywords:
InflammationMyD88Myocardial infarctionT3T4

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Area of Science:

  • Cardiology
  • Endocrinology
  • Molecular Biology

Background:

  • Myocardial infarction (MI) induces oxidative stress and activates the TLR4/NF-κβ inflammatory pathway.
  • Thyroid hormones (TH) are recognized for their cardioprotective effects post-MI.
  • The impact of TH on the TLR4/NF-κβ pathway in the infarcted heart remains uninvestigated.

Purpose of the Study:

  • To investigate the effect of thyroid hormones on the TLR4/NF-κβ pathway following myocardial infarction.
  • To determine if TH modulate inflammatory responses and oxidative stress markers in the infarcted heart.

Main Methods:

  • Male Wistar rats were divided into Sham-operated (SHAM), Sham+TH (SHAMT), Myocardial Infarction (AMI), and MI+TH (AMIT) groups.
  • TH (T4 and T3) were administered orally for 12 days.
  • Cardiac function was assessed via echocardiography, followed by biochemical and molecular analyses of left ventricular tissue.

Main Results:

  • Thyroid hormones significantly modulated TLR4/NF-κβ expression in infarcted rat hearts.
  • TH treatment led to a decrease in xanthine oxidase expression.
  • These molecular changes correlated with improved cardiac function after infarction.

Conclusions:

  • Thyroid hormones exert cardioprotective effects post-myocardial infarction.
  • The beneficial actions of TH involve the modulation of the TLR4/NF-κβ inflammatory pathway.
  • TH demonstrate anti-inflammatory properties that contribute to cardiac recovery after infarction.