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

被引：21

作者：

de Castro, Alexandre Luz ^{[1
,2
]}

Fernandes, Rafael Oliveira ^{[1
]}

Ortiz, Vanessa D. ^{[1
]}

Campos, Cristina ^{[1
]}

Bonetto, Jessica H. P. ^{[1
]}

Fernandes, Tania Regina G. ^{[1
]}

Conzatti, Adriana ^{[1
]}

Siqueira, Rafaela ^{[1
]}

Tavares, Angela Vicente ^{[1
,2
]}

Bello-Klein, Adriane ^{[1
]}

da Rosa Araujo, Alex Sander ^{[2
]}

机构：

[1] Fed Univ Rio Grande do Sul UFRGS, Lab Cardiovasc Physiol & React Oxygen Species, Physiol Dept, Inst Basic Hlth Sci ICBS, Sarmento Leite St 500, BR-90050170 Porto Alegre, RS, Brazil

[2] Ctr Univ Ritter Reis Uniritter, Orfanotrofio St 555, BR-90840440 Porto Alegre, RS, Brazil

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2018年 / 461卷 / 0C期

关键词：

T3; T4; MyD88; Inflammation; Myocardial infarction; ACUTE MYOCARDIAL-INFARCTION; FACTOR-KAPPA-B; CONGESTIVE-HEART-FAILURE; OXIDATIVE STRESS; INFLAMMATORY RESPONSE; DIABETIC MYOCARDIUM; REPLACEMENT THERAPY; RECEPTOR ALPHA-1; CARDIAC-FUNCTION; POTENTIAL ROLE;

D O I：

10.1016/j.mce.2017.09.003

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Myocardial infarction leads to oxidative stress and promotes activation of the TLR4/NF-kappa beta 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-kappa beta 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 mu g 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/NIF-kappa beta 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. (C) 2017 Elsevier B.V. All rights reserved.

引用

页码：132 / 142

页数：11

共 52 条

[21] ELEVATED CIRCULATING LEVELS OF TUMOR-NECROSIS-FACTOR IN SEVERE CHRONIC HEART-FAILURE [J].