Cardioprotective effects of thyroid hormones in a rat model of myocardial infarction are associated with oxidative stress reduction

•This study evaluated thyroid hormones effects in oxidative stress after infarction.•T3 and T4 administration reduced ROS levels induced by myocardial infarction.•This treatment also normalized cardiac redox status and prevented lipid peroxidation.•This was associated with improved cardiac remodelin...

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Published in:	Molecular and cellular endocrinology Vol. 391; no. 1-2; pp. 22 - 29
Main Authors:	de Castro, Alexandre Luz, Tavares, Angela Vicente, Campos, Cristina, Fernandes, Rafael Oliveira, Siqueira, Rafaela, Conzatti, Adriana, Bicca, Amanda M., Fernandes, Tânia Regina G., Sartório, Carmem L., Schenkel, Paulo Cavalheiro, Belló-Klein, Adriane, da Rosa Araujo, Alex Sander
Format:	Journal Article
Language:	English
Published:	Ireland Elsevier Ireland Ltd 25-06-2014
Subjects:	Animals Cardiomegaly - drug therapy Cardiomegaly - metabolism Cardiomegaly - physiopathology Cardiotonic Agents - pharmacology Catalase - metabolism Cellular Disease Models, Animal Failure Glutathione Disulfide - antagonists & inhibitors Glutathione Disulfide - metabolism Glutathione Peroxidase - metabolism Heart Heart - drug effects Heart - physiopathology Hormones Hydrogen Peroxide - antagonists & inhibitors Hydrogen Peroxide - metabolism Infarction Lipid Peroxidation - drug effects Male Mathematical models Myocardial Infarction - drug therapy Myocardial Infarction - metabolism Myocardial Infarction - physiopathology Oxidative Stress - drug effects Rats Rats, Wistar Reactive oxygen species Reactive Oxygen Species - antagonists & inhibitors Reactive Oxygen Species - metabolism Redox balance Stresses Superoxide Dismutase - metabolism Thyroxine - pharmacology Triiodothyronine - pharmacology T4 Redox balance Reactive oxygen species T3
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Summary:	•This study evaluated thyroid hormones effects in oxidative stress after infarction.•T3 and T4 administration reduced ROS levels induced by myocardial infarction.•This treatment also normalized cardiac redox status and prevented lipid peroxidation.•This was associated with improved cardiac remodeling after the ischemic injury.•Thus oxidative stress may have a relevant part in T3 and T4 cardioprotective effects. Reactive oxygen species (ROS) are involved with progression from infarction to heart failure. Studies show that thyroid hormones (TH) present cardioprotective effects. This study aims to evaluate whether TH effects after infarction are associated to redox balance modulation. Male Wistar rats were divided into four groups: Sham-operated (SHAM), infarcted (AMI), sham-operated+TH (SHAMT), and infarcted+TH (AMIT). During 26days, animals received T3 (2μg/100g/day) and T4 (8μg/100g/day) by gavage. Echocardiographic parameters were assessed and heart tissue was collected to biochemical analysis. AMIT rats presented absence of lung congestion, less cardiac dilatation, and normalization in myocardial performance index, compared with AMI. AMI rats presented an increase in hydrogen peroxide levels and in lipid peroxidation and a decrease in GSH/GSSG. TH prevented these alterations in AMIT. In conclusion, TH seem to reduce the levels of ROS, preventing oxidative stress, and improving cardiac function in infarcted rats.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1
ISSN:	0303-7207 1872-8057
DOI:	10.1016/j.mce.2014.04.010