Ortiz Vanessa D, de Castro Alexandre L, Campos Cristina, Fernandes Rafael O, Bonetto Jéssica H P, Siqueira Rafaela, Conzatti Adriana, Fernandes Tânia R G, Belló-Klein Adriane, Araujo Alex S R
Laboratory of Cardiovascular Physiology and Reactive Oxygen Species, Physiology Department, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.
Laboratory of Cardiovascular Physiology and Reactive Oxygen Species, Physiology Department, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil; Centro Universitário Ritter dos Reis (Uniritter), Porto Alegre, Rio Grande do Sul, Brazil.
Eur J Pharmacol. 2016 Nov 15;791:788-793. doi: 10.1016/j.ejphar.2016.10.022. Epub 2016 Oct 18.
Studies have shown a cardioprotective role of thyroid hormones (THs) in cardiac remodeling after acute myocardial infarction (MI). However, there is no data in the literature examining the influence of TH administration on the aortic tissue in an animal model of MI. This study aimed to evaluate the effects of thyroid hormones on the aorta after MI. Male Wistar rats were divided into a sham group (SHAM), infarcted group (AMI), sham+TH (SHAMT) and AMI+TH (AMIT). After MI, the animals received T3 and T4 (2 and 8μg/100g/day, respectively) by oral gavage for 12 days. Later, the animals underwent echocardiography and euthanasia and the aorta was collected for molecular and biochemical analysis. T3 and T4 administration increased the expression of the pro-angiogenic proteins vascular endothelial growth factor (VEGF) and hypoxia inducible factor 1α (HIF-1α) in the aorta of AMIT rats when compared with AMI. With respect to TH receptors, AMI rats presented a decrease in TRβ levels, which was prevented by the hormonal administration. In AMIT rats, both TRα and TRβ levels were increased when compared with the AMI group. Reactive oxygen species levels and NADPH oxidase activity were decreased in both treated groups when compared with the non-treated animals. TH administration after MI may improve angiogenic signaling in the aorta as well as the responsiveness of this vessel to T3 and T4. These positive effects in the aorta may result in additional protection for the cardiovascular system in the context of cardiac ischaemic injury.
研究表明，甲状腺激素（THs）在急性心肌梗死（MI）后的心脏重塑中具有心脏保护作用。然而，文献中尚无关于在MI动物模型中给予TH对主动脉组织影响的数据。本研究旨在评估甲状腺激素对MI后主动脉的影响。将雄性Wistar大鼠分为假手术组（SHAM）、梗死组（AMI）、假手术+TH组（SHAMT）和AMI+TH组（AMIT）。MI后，动物通过灌胃分别接受T3和T4（分别为2和8μg/100g/天），持续12天。之后，对动物进行超声心动图检查并实施安乐死，收集主动脉用于分子和生化分析。与AMI组相比，给予T3和T4可增加AMIT组大鼠主动脉中促血管生成蛋白血管内皮生长因子（VEGF）和缺氧诱导因子1α（HIF-1α）的表达。关于TH受体，AMI大鼠的TRβ水平降低，而激素给药可防止这种降低。与AMI组相比。AMIT组大鼠的TRα和TRβ水平均升高。与未治疗的动物相比，两个治疗组的活性氧水平和NADPH氧化酶活性均降低。MI后给予TH可能改善主动脉中的血管生成信号以及该血管对T3和T4的反应性。在心脏缺血性损伤的情况下，主动脉中的这些积极作用可能会为心血管系统带来额外的保护。
