Corssac Giana B, de Castro Alexandre L, Tavares Angela V, Campos Cristina, Fernandes Rafael O, Ortiz Vanessa D, Siqueira Rafaela, Fernandes Tânia Regina G, Belló-Klein Adriane, Araujo Alex Sander 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.
Life Sci. 2016 Feb 1;146:109-16. doi: 10.1016/j.lfs.2015.12.052. Epub 2016 Jan 4.
Right ventricle (RV) dysfunction post-myocardial infarction (MI) was associated with a worsened prognosis. In this scenario, reactive oxygen species (ROS) are related with the progression from MI to heart failure. Previous work showed that thyroid hormones (TH) are cardioprotective after MI.
This study aims to investigate the effect of T3 and T4 administration on oxidative stress and angiogenesis parameters in the RV after MI.
Wistar rats were allocated into four groups: Sham-operated (SHAM), infarcted (AMI), sham-operated + TH (SHAMT), and infarcted+TH (AMIT). The treated groups received T3 (2 μg/100g/day) and T4 (8 μg/100g/day) by gavage for 26 days. After this, echocardiographic analysis was performed and the RV was collected to western blot and biochemical analysis.
Infarcted treated rats showed RV hypertrophy compared with AMI and SHAMT. Hydrogen peroxide levels were decrease and SOD activity and expression were increased in the infarcted treated rats. Besides that, the hormonal administration increased eNOS expression and prevented the reduction of VEGF levels in AMIT rats.
In conclusion, TH seems to improve oxidative stress parameters, to promote physiological hypertrophy and to increase the expression of proteins involved with angiogenesis in the right heart.
心肌梗死后右心室(RV)功能障碍与预后恶化相关。在这种情况下,活性氧(ROS)与心肌梗死向心力衰竭的进展有关。先前的研究表明,甲状腺激素(TH)在心肌梗死后具有心脏保护作用。
本研究旨在探讨给予T3和T4对心肌梗死后右心室氧化应激和血管生成参数的影响。
将Wistar大鼠分为四组:假手术组(SHAM)、梗死组(AMI)、假手术+甲状腺激素组(SHAMT)和梗死+甲状腺激素组(AMIT)。治疗组通过灌胃给予T3(2μg/100g/天)和T4(8μg/100g/天),持续26天。此后,进行超声心动图分析,并收集右心室进行蛋白质印迹和生化分析。
与AMI组和SHAMT组相比,梗死治疗组大鼠出现右心室肥厚。梗死治疗组大鼠的过氧化氢水平降低,超氧化物歧化酶(SOD)活性和表达增加。此外,激素给药增加了AMIT组大鼠的内皮型一氧化氮合酶(eNOS)表达,并防止了血管内皮生长因子(VEGF)水平的降低。
总之,甲状腺激素似乎可以改善氧化应激参数,促进生理性肥厚,并增加右心与血管生成相关蛋白质的表达。