Related Experiment Video
Updated: Feb 23, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
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.
Abstract:
Myocardial infarction leads to oxidative stress and promotes activation of the TLR4/NF-κβ proinflammatory pathway. Thyroid hormones (TH) are known to be cardioprotective after infarction. However, there are no studies evaluating whether TH could modulate this pathway in the heart. This study aimed to verify the effect of thyroid hormones on the TLR4/NF-κβ pathway after myocardial infarction. Male Wistar rats were allocated into the following groups: Sham-operated (SHAM), sham-operated + TH (SHAMT), infarcted (AMI) and infarcted + TH (AMIT). The treated rats received T4 and T3 (8 and 2 μg 100 g-1 day-1) for 12 days by gavage. Subsequently, the animals were evaluated by echocardiography and euthanized, and the left ventricle was collected for biochemical and molecular analyses. TH modulates TLR4/NF-κβ expression in the infarcted hearts of rats and decreases xanthine oxidase expression. These effects were related to cardiac functional improvement after infarction. The cardioprotective effects of T3 and T4 seem to involve an anti-inflammatory action.
