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

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

Abstract 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..

Medienart:	E-Artikel

Erscheinungsjahr:	2015
Erschienen:	2015

Enthalten in:	Zur Gesamtaufnahme - volume:408
Enthalten in:	Molecular and cellular biochemistry - 408(2015), 1-2 vom: 10. Juli, Seite 235-243

Sprache:	Englisch

Beteiligte Personen:	de Castro, Alexandre Luz [VerfasserIn] Tavares, Angela Vicente [VerfasserIn] Fernandes, Rafael Oliveira [VerfasserIn] Campos, Cristina [VerfasserIn] Conzatti, Adriana [VerfasserIn] Siqueira, Rafaela [VerfasserIn] Fernandes, Tânia Regina G. [VerfasserIn] Schenkel, Paulo Cavalheiro [VerfasserIn] Sartório, Carmem L. [VerfasserIn] Llesuy, Susana [VerfasserIn] Belló-Klein, Adriane [VerfasserIn] da Rosa Araujo, Alex Sander [VerfasserIn]

Links:	Volltext [lizenzpflichtig]

BKL:	44.00$jMedizin: Allgemeines
Themen:	Heart failure Nitric oxide Oxidative stress Thyroid hormones

Anmerkungen:	© Springer Science+Business Media New York 2015

doi:	10.1007/s11010-015-2501-4

funding:
Förderinstitution / Projekttitel:

PPN (Katalog-ID):	OLC2081097710

Internformat


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520			\|a Abstract 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.
650		4	\|a Heart failure
650		4	\|a Thyroid hormones
650		4	\|a Oxidative stress
650		4	\|a Nitric oxide
700	1		\|a Tavares, Angela Vicente \|4 aut
700	1		\|a Fernandes, Rafael Oliveira \|4 aut
700	1		\|a Campos, Cristina \|4 aut
700	1		\|a Conzatti, Adriana \|4 aut
700	1		\|a Siqueira, Rafaela \|4 aut
700	1		\|a Fernandes, Tânia Regina G. \|4 aut
700	1		\|a Schenkel, Paulo Cavalheiro \|4 aut
700	1		\|a Sartório, Carmem L. \|4 aut
700	1		\|a Llesuy, Susana \|4 aut
700	1		\|a Belló-Klein, Adriane \|4 aut
700	1		\|a da Rosa Araujo, Alex Sander \|4 aut
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773	1	8	\|g volume:408 \|g year:2015 \|g number:1-2 \|g day:10 \|g month:07 \|g pages:235-243
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T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats

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