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Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation
Epidemiologic investigations have shown that exercise reduces morbidity and mortality from coronary artery disease. In this study, using a rat model, we attempted to determine whether exercise can reduce ischemic injury to the heart and elucidate a mechanism for the cardioprotective effect of exerci...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1999
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193084/ https://www.ncbi.nlm.nih.gov/pubmed/10359573 |
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author | Yamashita, Nobushige Hoshida, Shiro Otsu, Kinya Asahi, Michio Kuzuya, Tsunehiko Hori, Masatsugu |
author_facet | Yamashita, Nobushige Hoshida, Shiro Otsu, Kinya Asahi, Michio Kuzuya, Tsunehiko Hori, Masatsugu |
author_sort | Yamashita, Nobushige |
collection | PubMed |
description | Epidemiologic investigations have shown that exercise reduces morbidity and mortality from coronary artery disease. In this study, using a rat model, we attempted to determine whether exercise can reduce ischemic injury to the heart and elucidate a mechanism for the cardioprotective effect of exercise. Results showed that exercise significantly reduced the magnitude of a myocardial infarction in biphasic manner. The time course for cardioprotection resembled that of the change in manganese superoxide dismutase (Mn-SOD) activity. The administration of the antisense oligodeoxyribonucleotide to Mn-SOD abolished the expected decrease in infarct size. We showed that the level of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) increased after exercise. The simultaneous administration of the neutralizing antibodies to the cytokines abolished the exercise-induced cardioprotection and the activation of Mn-SOD. Furthermore, TNF-α can mimic the biphasic pattern of cardioprotection and activation of Mn-SOD. An antioxidant completely abolished cardioprotection and the activation of Mn-SOD by exercise or the injection of TNF-α as well as exercise-induced increase in TNF-α and IL-1β. The production of reactive oxygen species and endogenous TNF-α and IL-1β induced by exercise leads to the activation of Mn-SOD, which plays major roles in the acquisition of biphasic cardioprotection against ischemia/reperfusion injury in rats. |
format | Text |
id | pubmed-2193084 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1999 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21930842008-04-16 Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation Yamashita, Nobushige Hoshida, Shiro Otsu, Kinya Asahi, Michio Kuzuya, Tsunehiko Hori, Masatsugu J Exp Med Articles Epidemiologic investigations have shown that exercise reduces morbidity and mortality from coronary artery disease. In this study, using a rat model, we attempted to determine whether exercise can reduce ischemic injury to the heart and elucidate a mechanism for the cardioprotective effect of exercise. Results showed that exercise significantly reduced the magnitude of a myocardial infarction in biphasic manner. The time course for cardioprotection resembled that of the change in manganese superoxide dismutase (Mn-SOD) activity. The administration of the antisense oligodeoxyribonucleotide to Mn-SOD abolished the expected decrease in infarct size. We showed that the level of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) increased after exercise. The simultaneous administration of the neutralizing antibodies to the cytokines abolished the exercise-induced cardioprotection and the activation of Mn-SOD. Furthermore, TNF-α can mimic the biphasic pattern of cardioprotection and activation of Mn-SOD. An antioxidant completely abolished cardioprotection and the activation of Mn-SOD by exercise or the injection of TNF-α as well as exercise-induced increase in TNF-α and IL-1β. The production of reactive oxygen species and endogenous TNF-α and IL-1β induced by exercise leads to the activation of Mn-SOD, which plays major roles in the acquisition of biphasic cardioprotection against ischemia/reperfusion injury in rats. The Rockefeller University Press 1999-06-07 /pmc/articles/PMC2193084/ /pubmed/10359573 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Yamashita, Nobushige Hoshida, Shiro Otsu, Kinya Asahi, Michio Kuzuya, Tsunehiko Hori, Masatsugu Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation |
title | Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation |
title_full | Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation |
title_fullStr | Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation |
title_full_unstemmed | Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation |
title_short | Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation |
title_sort | exercise provides direct biphasic cardioprotection via manganese superoxide dismutase activation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193084/ https://www.ncbi.nlm.nih.gov/pubmed/10359573 |
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