Previous exercise training increases levels of ppar-alpha in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Outros Autores: | , , , , , , |
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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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 |
_version_ |
1814268435587137536 |