Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response

Detalhes bibliográficos
Autor(a) principal: Higuchi Santos, Marilia Harumi
Data de Publicação: 2016
Outros Autores: Higuchi, Maria de Lourdes, Tucci, Paulo J. F. [UNIFESP], Garavelo, Sherrira M., Reis, Marcia M., Antonio, Ednei L. [UNIFESP], Serra, Andrey J., Maranhao, Raul Cavalcante
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.6061/clinics/2016(03)08
http://repositorio.unifesp.br/handle/11600/49517
Resumo: OBJECTIVE: Exercise is a protective factor for cardiovascular morbidity and mortality, with unclear mechanisms. Changing the myocardial metabolism causes harmful consequences for heart function and exercise contributes to metabolic adjustment modulation. Peroxisome proliferator-activated receptors (PPARs) are also myocardium metabolism regulators capable of decreasing the inflammatory response. We hypothesized that PPAR-alpha is involved in the beneficial effects of previous exercise on myocardial infarction (MI) and cardiac function, changing the expression of metabolic and inflammatory response regulators and reducing myocardial apoptosis, which partially explains the better outcome. METHODS AND RESULTS: Exercised rats engaged in swimming sessions for 60 min/day, 5 days/week, for 8 weeks. Both the exercised rats and sedentary rats were randomized to MI surgery and followed for 1 week (EI1 or SI1) or 4 weeks (EI4 or SI4) of healing or to sham groups. Echocardiography was employed to detect left ventricular function and the infarct size. Additionally, the TUNEL technique was used to assess apoptosis and immunohistochemistry was used to quantitatively analyze the PPAR-alpha, TNF-alpha and NF-kappa B antigens in the infarcted and non-infarcted myocardium. MI-related mortality was higher in SI4 than in EI4 (25% vs 12%), without a difference in MI size. SI4 exhibited a lower shortening fraction than EI4 did (24% vs 35%) and a higher apoptosis/area rate (3.97 +/- 0.61 vs 1.90 +/- 1.82) in infarcted areas (both p=0.001). Immunohistochemistry also revealed higher TNF-alpha levels in SI1 than in EI1 (9.59 vs 4.09, p<0.001) in infarcted areas. In non-infarcted areas, EI4 showed higher levels of TNF-alpha and positive correlations between PPAR-alpha and NF-kappa B (r=0.75, p=0.02), in contrast to SI4 (r=0.05, p=0.87). CONCLUSION: Previously exercised animals had better long-term ventricular function post-MI, in addition to lower levels of local inflammatory markers and less myocardial apoptosis, which seemed to be related to the presence of PPAR-alpha.
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spelling Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory responseExercise TrainingMyocardial InfarctionPpar-AlphaApoptosisInflammationAcute Myocardial-InfarctionActivated Receptor-AlphaLeft-Ventricular FunctionImprovesHypertrophyProtectionDiseaseDeathOBJECTIVE: Exercise is a protective factor for cardiovascular morbidity and mortality, with unclear mechanisms. Changing the myocardial metabolism causes harmful consequences for heart function and exercise contributes to metabolic adjustment modulation. Peroxisome proliferator-activated receptors (PPARs) are also myocardium metabolism regulators capable of decreasing the inflammatory response. We hypothesized that PPAR-alpha is involved in the beneficial effects of previous exercise on myocardial infarction (MI) and cardiac function, changing the expression of metabolic and inflammatory response regulators and reducing myocardial apoptosis, which partially explains the better outcome. METHODS AND RESULTS: Exercised rats engaged in swimming sessions for 60 min/day, 5 days/week, for 8 weeks. Both the exercised rats and sedentary rats were randomized to MI surgery and followed for 1 week (EI1 or SI1) or 4 weeks (EI4 or SI4) of healing or to sham groups. Echocardiography was employed to detect left ventricular function and the infarct size. Additionally, the TUNEL technique was used to assess apoptosis and immunohistochemistry was used to quantitatively analyze the PPAR-alpha, TNF-alpha and NF-kappa B antigens in the infarcted and non-infarcted myocardium. MI-related mortality was higher in SI4 than in EI4 (25% vs 12%), without a difference in MI size. SI4 exhibited a lower shortening fraction than EI4 did (24% vs 35%) and a higher apoptosis/area rate (3.97 +/- 0.61 vs 1.90 +/- 1.82) in infarcted areas (both p=0.001). Immunohistochemistry also revealed higher TNF-alpha levels in SI1 than in EI1 (9.59 vs 4.09, p<0.001) in infarcted areas. In non-infarcted areas, EI4 showed higher levels of TNF-alpha and positive correlations between PPAR-alpha and NF-kappa B (r=0.75, p=0.02), in contrast to SI4 (r=0.05, p=0.87). CONCLUSION: Previously exercised animals had better long-term ventricular function post-MI, in addition to lower levels of local inflammatory markers and less myocardial apoptosis, which seemed to be related to the presence of PPAR-alpha.Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Instituto do Coração (InCor), Laboratório de Patologia Cardíaca, São Paulo/, SP, BrazilUniversidade Federal de São Paulo (UNIFESP), Cardiologia, São Paulo, SP, BrazilUniversidade Federal de São Paulo (UNIFESP), Fisiologia Cardíaca, São Paulo, SP, BrazilUniversidade Nove Julho, Programa de Pós Graduação em Biofotônica Aplicada às Ciências da Saúde, São Paulo/, SP, BrazilUniversidade Federal de São Paulo (UNIFESP), Cardiologia, São Paulo, SP, BrazilUniversidade Federal de São Paulo (UNIFESP), Fisiologia Cardíaca, São Paulo, SP, BrazilWeb of ScienceFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [06/50489-2]Zerbini FoundationFAPESP: 06/50489-2Hospital clinicas, univ sao paulo2019-01-21T10:29:59Z2019-01-21T10:29:59Z2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion163-168http://dx.doi.org/10.6061/clinics/2016(03)08Clinics. Sao paulo, v. 71, n. 3, p. 163-168, 2016.10.6061/clinics/2016(03)08S1807-59322016000300163.pdf1807-5932S1807-59322016000300163http://repositorio.unifesp.br/handle/11600/49517WOS:000374484800008engClinicsinfo:eu-repo/semantics/openAccessHiguchi Santos, Marilia HarumiHiguchi, Maria de LourdesTucci, Paulo J. F. [UNIFESP]Garavelo, Sherrira M.Reis, Marcia M.Antonio, Ednei L. [UNIFESP]Serra, Andrey J.Maranhao, Raul Cavalcantereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2022-02-09T10:37:25Zoai:repositorio.unifesp.br/:11600/49517Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652022-02-09T10:37:25Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
title Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
spellingShingle Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
Higuchi Santos, Marilia Harumi
Exercise Training
Myocardial Infarction
Ppar-Alpha
Apoptosis
InflammationAcute Myocardial-Infarction
Activated Receptor-Alpha
Left-Ventricular Function
Improves
Hypertrophy
Protection
Disease
Death
title_short Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
title_full Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
title_fullStr Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
title_full_unstemmed Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
title_sort Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
author Higuchi Santos, Marilia Harumi
author_facet Higuchi Santos, Marilia Harumi
Higuchi, Maria de Lourdes
Tucci, Paulo J. F. [UNIFESP]
Garavelo, Sherrira M.
Reis, Marcia M.
Antonio, Ednei L. [UNIFESP]
Serra, Andrey J.
Maranhao, Raul Cavalcante
author_role author
author2 Higuchi, Maria de Lourdes
Tucci, Paulo J. F. [UNIFESP]
Garavelo, Sherrira M.
Reis, Marcia M.
Antonio, Ednei L. [UNIFESP]
Serra, Andrey J.
Maranhao, Raul Cavalcante
author2_role author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Higuchi Santos, Marilia Harumi
Higuchi, Maria de Lourdes
Tucci, Paulo J. F. [UNIFESP]
Garavelo, Sherrira M.
Reis, Marcia M.
Antonio, Ednei L. [UNIFESP]
Serra, Andrey J.
Maranhao, Raul Cavalcante
dc.subject.por.fl_str_mv Exercise Training
Myocardial Infarction
Ppar-Alpha
Apoptosis
InflammationAcute Myocardial-Infarction
Activated Receptor-Alpha
Left-Ventricular Function
Improves
Hypertrophy
Protection
Disease
Death
topic Exercise Training
Myocardial Infarction
Ppar-Alpha
Apoptosis
InflammationAcute Myocardial-Infarction
Activated Receptor-Alpha
Left-Ventricular Function
Improves
Hypertrophy
Protection
Disease
Death
description OBJECTIVE: Exercise is a protective factor for cardiovascular morbidity and mortality, with unclear mechanisms. Changing the myocardial metabolism causes harmful consequences for heart function and exercise contributes to metabolic adjustment modulation. Peroxisome proliferator-activated receptors (PPARs) are also myocardium metabolism regulators capable of decreasing the inflammatory response. We hypothesized that PPAR-alpha is involved in the beneficial effects of previous exercise on myocardial infarction (MI) and cardiac function, changing the expression of metabolic and inflammatory response regulators and reducing myocardial apoptosis, which partially explains the better outcome. METHODS AND RESULTS: Exercised rats engaged in swimming sessions for 60 min/day, 5 days/week, for 8 weeks. Both the exercised rats and sedentary rats were randomized to MI surgery and followed for 1 week (EI1 or SI1) or 4 weeks (EI4 or SI4) of healing or to sham groups. Echocardiography was employed to detect left ventricular function and the infarct size. Additionally, the TUNEL technique was used to assess apoptosis and immunohistochemistry was used to quantitatively analyze the PPAR-alpha, TNF-alpha and NF-kappa B antigens in the infarcted and non-infarcted myocardium. MI-related mortality was higher in SI4 than in EI4 (25% vs 12%), without a difference in MI size. SI4 exhibited a lower shortening fraction than EI4 did (24% vs 35%) and a higher apoptosis/area rate (3.97 +/- 0.61 vs 1.90 +/- 1.82) in infarcted areas (both p=0.001). Immunohistochemistry also revealed higher TNF-alpha levels in SI1 than in EI1 (9.59 vs 4.09, p<0.001) in infarcted areas. In non-infarcted areas, EI4 showed higher levels of TNF-alpha and positive correlations between PPAR-alpha and NF-kappa B (r=0.75, p=0.02), in contrast to SI4 (r=0.05, p=0.87). CONCLUSION: Previously exercised animals had better long-term ventricular function post-MI, in addition to lower levels of local inflammatory markers and less myocardial apoptosis, which seemed to be related to the presence of PPAR-alpha.
publishDate 2016
dc.date.none.fl_str_mv 2016
2019-01-21T10:29:59Z
2019-01-21T10:29:59Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.6061/clinics/2016(03)08
Clinics. Sao paulo, v. 71, n. 3, p. 163-168, 2016.
10.6061/clinics/2016(03)08
S1807-59322016000300163.pdf
1807-5932
S1807-59322016000300163
http://repositorio.unifesp.br/handle/11600/49517
WOS:000374484800008
url http://dx.doi.org/10.6061/clinics/2016(03)08
http://repositorio.unifesp.br/handle/11600/49517
identifier_str_mv Clinics. Sao paulo, v. 71, n. 3, p. 163-168, 2016.
10.6061/clinics/2016(03)08
S1807-59322016000300163.pdf
1807-5932
S1807-59322016000300163
WOS:000374484800008
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Clinics
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 163-168
dc.publisher.none.fl_str_mv Hospital clinicas, univ sao paulo
publisher.none.fl_str_mv Hospital clinicas, univ sao paulo
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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