T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats

Autores
de Castro, Alexandre Luz; Tavares, Angela Vicente; Fernandes, Rafael Oliveira; Campos, Cristina; Conzatti, Adriana; Siqueira, Rafaela; Fernandes, Tânia Regina G.; Schenkel, Paulo Cavalheiro; Sartório, Carmem L.; Llesuy, Susana Francisca; Belló Klein, Adriane; da Rosa Araujo, Alex Sander
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Myocardial infarction leads to a reduction in nitric oxide (NO) bioavailability and an increase in reactive oxygen species (ROS) levels. This scenario has been shown to be detrimental to the heart. Recent studies have shown that thyroid hormone (TH) administration presents positive effects after ischaemic injury. Based on this, the aim of this study was to evaluate the effect of TH on NO bioavailability as well as on endothelial nitric oxide synthase (eNOS) expression after myocardial infarction. Male Wistar rats were divided into three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted + TH (AMIT). During 26 days, the AMIT group received T3 and T4 (2 and 8 µg/100 g/day, respectively) by gavage, while SHAM and AMI rats received saline. After this, the rats underwent echocardiographic analysis were sacrificed, and the left ventricle was collected for biochemical and molecular analysis. Statistical analysis: one-way ANOVA with Student–Newman–Keuls post test. AMI rats presented a 38 % increase in ROS levels. TH administration prevented these alterations in AMIT rats. The AMIT group presented an increase in eNOS expression, in NOS activity and in nitrite levels. TH administration also increased PGC-1α expression in the AMIT group. In conclusion, TH effects seem to involve a modulation of eNOS expression and an improvement in NO bioavailability in the infarcted heart.
Fil: de Castro, Alexandre Luz. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Tavares, Angela Vicente. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Fernandes, Rafael Oliveira. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Campos, Cristina. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Conzatti, Adriana. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Siqueira, Rafaela. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Fernandes, Tânia Regina G.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Schenkel, Paulo Cavalheiro. Universidade Federal de Pelotas; Brasil
Fil: Sartório, Carmem L.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Llesuy, Susana Francisca. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Belló Klein, Adriane. Universidade Federal do Rio Grande do Sul; Brasil
Fil: da Rosa Araujo, Alex Sander. Universidade Federal do Rio Grande do Sul; Brasil
Materia
Heart Failure
Nitric Oxide
Oxidative Stress
Thyroid Hormones
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/38961
Acceder
id CONICETDig_830e76fdbd939f7ebb0724816f3da80a
oai_identifier_str oai:ri.conicet.gov.ar:11336/38961
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted ratsde Castro, Alexandre LuzTavares, Angela VicenteFernandes, Rafael OliveiraCampos, CristinaConzatti, AdrianaSiqueira, RafaelaFernandes, Tânia Regina G.Schenkel, Paulo CavalheiroSartório, Carmem L.Llesuy, Susana FranciscaBelló Klein, Adrianeda Rosa Araujo, Alex SanderHeart FailureNitric OxideOxidative StressThyroid Hormoneshttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Myocardial infarction leads to a reduction in nitric oxide (NO) bioavailability and an increase in reactive oxygen species (ROS) levels. This scenario has been shown to be detrimental to the heart. Recent studies have shown that thyroid hormone (TH) administration presents positive effects after ischaemic injury. Based on this, the aim of this study was to evaluate the effect of TH on NO bioavailability as well as on endothelial nitric oxide synthase (eNOS) expression after myocardial infarction. Male Wistar rats were divided into three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted + TH (AMIT). During 26 days, the AMIT group received T3 and T4 (2 and 8 µg/100 g/day, respectively) by gavage, while SHAM and AMI rats received saline. After this, the rats underwent echocardiographic analysis were sacrificed, and the left ventricle was collected for biochemical and molecular analysis. Statistical analysis: one-way ANOVA with Student–Newman–Keuls post test. AMI rats presented a 38 % increase in ROS levels. TH administration prevented these alterations in AMIT rats. The AMIT group presented an increase in eNOS expression, in NOS activity and in nitrite levels. TH administration also increased PGC-1α expression in the AMIT group. In conclusion, TH effects seem to involve a modulation of eNOS expression and an improvement in NO bioavailability in the infarcted heart.Fil: de Castro, Alexandre Luz. Universidade Federal do Rio Grande do Sul; BrasilFil: Tavares, Angela Vicente. Universidade Federal do Rio Grande do Sul; BrasilFil: Fernandes, Rafael Oliveira. Universidade Federal do Rio Grande do Sul; BrasilFil: Campos, Cristina. Universidade Federal do Rio Grande do Sul; BrasilFil: Conzatti, Adriana. Universidade Federal do Rio Grande do Sul; BrasilFil: Siqueira, Rafaela. Universidade Federal do Rio Grande do Sul; BrasilFil: Fernandes, Tânia Regina G.. Universidade Federal do Rio Grande do Sul; BrasilFil: Schenkel, Paulo Cavalheiro. Universidade Federal de Pelotas; BrasilFil: Sartório, Carmem L.. Universidade Federal do Rio Grande do Sul; BrasilFil: Llesuy, Susana Francisca. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Belló Klein, Adriane. Universidade Federal do Rio Grande do Sul; BrasilFil: da Rosa Araujo, Alex Sander. Universidade Federal do Rio Grande do Sul; BrasilSpringer2015-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/38961de Castro, Alexandre Luz; Tavares, Angela Vicente; Fernandes, Rafael Oliveira; Campos, Cristina; Conzatti, Adriana; et al.; T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats; Springer; Molecular and Cellular Biochemistry; 408; 1-2; 10-2015; 235-2430300-8177CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-015-2501-4info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-015-2501-4info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:05:06Zoai:ri.conicet.gov.ar:11336/38961instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:05:06.949CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
title T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
spellingShingle T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
de Castro, Alexandre Luz
Heart Failure
Nitric Oxide
Oxidative Stress
Thyroid Hormones
title_short T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
title_full T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
title_fullStr T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
title_full_unstemmed T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
title_sort T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats
dc.creator.none.fl_str_mv de Castro, Alexandre Luz
Tavares, Angela Vicente
Fernandes, Rafael Oliveira
Campos, Cristina
Conzatti, Adriana
Siqueira, Rafaela
Fernandes, Tânia Regina G.
Schenkel, Paulo Cavalheiro
Sartório, Carmem L.
Llesuy, Susana Francisca
Belló Klein, Adriane
da Rosa Araujo, Alex Sander
author de Castro, Alexandre Luz
author_facet de Castro, Alexandre Luz
Tavares, Angela Vicente
Fernandes, Rafael Oliveira
Campos, Cristina
Conzatti, Adriana
Siqueira, Rafaela
Fernandes, Tânia Regina G.
Schenkel, Paulo Cavalheiro
Sartório, Carmem L.
Llesuy, Susana Francisca
Belló Klein, Adriane
da Rosa Araujo, Alex Sander
author_role author
author2 Tavares, Angela Vicente
Fernandes, Rafael Oliveira
Campos, Cristina
Conzatti, Adriana
Siqueira, Rafaela
Fernandes, Tânia Regina G.
Schenkel, Paulo Cavalheiro
Sartório, Carmem L.
Llesuy, Susana Francisca
Belló Klein, Adriane
da Rosa Araujo, Alex Sander
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Heart Failure
Nitric Oxide
Oxidative Stress
Thyroid Hormones
topic Heart Failure
Nitric Oxide
Oxidative Stress
Thyroid Hormones
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Myocardial infarction leads to a reduction in nitric oxide (NO) bioavailability and an increase in reactive oxygen species (ROS) levels. This scenario has been shown to be detrimental to the heart. Recent studies have shown that thyroid hormone (TH) administration presents positive effects after ischaemic injury. Based on this, the aim of this study was to evaluate the effect of TH on NO bioavailability as well as on endothelial nitric oxide synthase (eNOS) expression after myocardial infarction. Male Wistar rats were divided into three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted + TH (AMIT). During 26 days, the AMIT group received T3 and T4 (2 and 8 µg/100 g/day, respectively) by gavage, while SHAM and AMI rats received saline. After this, the rats underwent echocardiographic analysis were sacrificed, and the left ventricle was collected for biochemical and molecular analysis. Statistical analysis: one-way ANOVA with Student–Newman–Keuls post test. AMI rats presented a 38 % increase in ROS levels. TH administration prevented these alterations in AMIT rats. The AMIT group presented an increase in eNOS expression, in NOS activity and in nitrite levels. TH administration also increased PGC-1α expression in the AMIT group. In conclusion, TH effects seem to involve a modulation of eNOS expression and an improvement in NO bioavailability in the infarcted heart.
Fil: de Castro, Alexandre Luz. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Tavares, Angela Vicente. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Fernandes, Rafael Oliveira. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Campos, Cristina. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Conzatti, Adriana. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Siqueira, Rafaela. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Fernandes, Tânia Regina G.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Schenkel, Paulo Cavalheiro. Universidade Federal de Pelotas; Brasil
Fil: Sartório, Carmem L.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Llesuy, Susana Francisca. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Belló Klein, Adriane. Universidade Federal do Rio Grande do Sul; Brasil
Fil: da Rosa Araujo, Alex Sander. Universidade Federal do Rio Grande do Sul; Brasil
description Myocardial infarction leads to a reduction in nitric oxide (NO) bioavailability and an increase in reactive oxygen species (ROS) levels. This scenario has been shown to be detrimental to the heart. Recent studies have shown that thyroid hormone (TH) administration presents positive effects after ischaemic injury. Based on this, the aim of this study was to evaluate the effect of TH on NO bioavailability as well as on endothelial nitric oxide synthase (eNOS) expression after myocardial infarction. Male Wistar rats were divided into three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted + TH (AMIT). During 26 days, the AMIT group received T3 and T4 (2 and 8 µg/100 g/day, respectively) by gavage, while SHAM and AMI rats received saline. After this, the rats underwent echocardiographic analysis were sacrificed, and the left ventricle was collected for biochemical and molecular analysis. Statistical analysis: one-way ANOVA with Student–Newman–Keuls post test. AMI rats presented a 38 % increase in ROS levels. TH administration prevented these alterations in AMIT rats. The AMIT group presented an increase in eNOS expression, in NOS activity and in nitrite levels. TH administration also increased PGC-1α expression in the AMIT group. In conclusion, TH effects seem to involve a modulation of eNOS expression and an improvement in NO bioavailability in the infarcted heart.
publishDate 2015
dc.date.none.fl_str_mv 2015-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/38961
de Castro, Alexandre Luz; Tavares, Angela Vicente; Fernandes, Rafael Oliveira; Campos, Cristina; Conzatti, Adriana; et al.; T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats; Springer; Molecular and Cellular Biochemistry; 408; 1-2; 10-2015; 235-243
0300-8177
CONICET Digital
CONICET
url http://hdl.handle.net/11336/38961
identifier_str_mv de Castro, Alexandre Luz; Tavares, Angela Vicente; Fernandes, Rafael Oliveira; Campos, Cristina; Conzatti, Adriana; et al.; T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats; Springer; Molecular and Cellular Biochemistry; 408; 1-2; 10-2015; 235-243
0300-8177
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-015-2501-4
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-015-2501-4
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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