Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Acta Cirúrgica Brasileira (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502017000500376 |
Resumo: | Abstract Purpose: To investigate whether modulating GSK-3β could attenuate myocardial ischemia reperfusion injury (MIRI) induced acute lung injury (ALI) and analyze the underlying mechanism. Methods: Male SD rats were subjected to MIRI with or without myocardial ischemic post-conditioning in the presence or absence of GSK-3β inhibitor. GSK-3β inhibitor was injected peritoneally 10min before MIRI. Lung W/D weight ratio, MPO, PMNs, histopathological changes, TUNEL, Bax, Bcl-2, IL-6, IL-8, IL-10, GSK-3β, and caspase-3 were evaluated in the lung tissues of all rats. Results: After MIRI, lung injury was significantly increased manifested as significant morphological changes and increased leukocytes in the interstitial capillaries, Lung W/D ratio, MPO, and PMN in BALF, which was associated with enhanced inflammation evidenced by increased expressions of IL-6, IL-8 and reduced expression of IL-10. MIRI significantly increased cell apoptosis in the lung as increased levels of apoptotosis, Bax, cleaved caspase-3, and reduced expression of Bcl-2 was observed, which was concomitant with reduced p-GSK-3β. All these changes were reversed/prevented by ischemic post-conditioning, while these beneficial effects of ischemic post-conditioning were abolished by GSK-3β inhibition. Conclusion: Myocardial ischemia reperfusion injury induces acute lung injury by induction of inflammation and cell apoptosis. Ischemic post-conditioning protects the lung from ALI following MIRI by increasing p-GSK-3β. |
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Acta Cirúrgica Brasileira (Online) |
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Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3βMyocardial IschemiaMyocardial ReperfusionPost-conditioningAcute Lung InjuryRatsAbstract Purpose: To investigate whether modulating GSK-3β could attenuate myocardial ischemia reperfusion injury (MIRI) induced acute lung injury (ALI) and analyze the underlying mechanism. Methods: Male SD rats were subjected to MIRI with or without myocardial ischemic post-conditioning in the presence or absence of GSK-3β inhibitor. GSK-3β inhibitor was injected peritoneally 10min before MIRI. Lung W/D weight ratio, MPO, PMNs, histopathological changes, TUNEL, Bax, Bcl-2, IL-6, IL-8, IL-10, GSK-3β, and caspase-3 were evaluated in the lung tissues of all rats. Results: After MIRI, lung injury was significantly increased manifested as significant morphological changes and increased leukocytes in the interstitial capillaries, Lung W/D ratio, MPO, and PMN in BALF, which was associated with enhanced inflammation evidenced by increased expressions of IL-6, IL-8 and reduced expression of IL-10. MIRI significantly increased cell apoptosis in the lung as increased levels of apoptotosis, Bax, cleaved caspase-3, and reduced expression of Bcl-2 was observed, which was concomitant with reduced p-GSK-3β. All these changes were reversed/prevented by ischemic post-conditioning, while these beneficial effects of ischemic post-conditioning were abolished by GSK-3β inhibition. Conclusion: Myocardial ischemia reperfusion injury induces acute lung injury by induction of inflammation and cell apoptosis. Ischemic post-conditioning protects the lung from ALI following MIRI by increasing p-GSK-3β.Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia2017-05-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502017000500376Acta Cirúrgica Brasileira v.32 n.5 2017reponame:Acta Cirúrgica Brasileira (Online)instname:Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)instacron:SBDPC10.1590/s0102-865020170050000007info:eu-repo/semantics/openAccessGao,WenweiZhao,BoLiu,LianYuan,QuanWu,XiaojingXia,Zhongyuaneng2017-06-02T00:00:00Zoai:scielo:S0102-86502017000500376Revistahttps://www.bvs-vet.org.br/vetindex/periodicos/acta-cirurgica-brasileira/https://old.scielo.br/oai/scielo-oai.php||sgolden@terra.com.br0102-86501678-2674opendoar:2017-06-02T00:00Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)false |
dc.title.none.fl_str_mv |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β |
title |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β |
spellingShingle |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β Gao,Wenwei Myocardial Ischemia Myocardial Reperfusion Post-conditioning Acute Lung Injury Rats |
title_short |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β |
title_full |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β |
title_fullStr |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β |
title_full_unstemmed |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β |
title_sort |
Myocardial ischemic post-conditioning protects the lung against myocardial ischemia/reperfusion-induced damage by activating GSK-3β |
author |
Gao,Wenwei |
author_facet |
Gao,Wenwei Zhao,Bo Liu,Lian Yuan,Quan Wu,Xiaojing Xia,Zhongyuan |
author_role |
author |
author2 |
Zhao,Bo Liu,Lian Yuan,Quan Wu,Xiaojing Xia,Zhongyuan |
author2_role |
author author author author author |
dc.contributor.author.fl_str_mv |
Gao,Wenwei Zhao,Bo Liu,Lian Yuan,Quan Wu,Xiaojing Xia,Zhongyuan |
dc.subject.por.fl_str_mv |
Myocardial Ischemia Myocardial Reperfusion Post-conditioning Acute Lung Injury Rats |
topic |
Myocardial Ischemia Myocardial Reperfusion Post-conditioning Acute Lung Injury Rats |
description |
Abstract Purpose: To investigate whether modulating GSK-3β could attenuate myocardial ischemia reperfusion injury (MIRI) induced acute lung injury (ALI) and analyze the underlying mechanism. Methods: Male SD rats were subjected to MIRI with or without myocardial ischemic post-conditioning in the presence or absence of GSK-3β inhibitor. GSK-3β inhibitor was injected peritoneally 10min before MIRI. Lung W/D weight ratio, MPO, PMNs, histopathological changes, TUNEL, Bax, Bcl-2, IL-6, IL-8, IL-10, GSK-3β, and caspase-3 were evaluated in the lung tissues of all rats. Results: After MIRI, lung injury was significantly increased manifested as significant morphological changes and increased leukocytes in the interstitial capillaries, Lung W/D ratio, MPO, and PMN in BALF, which was associated with enhanced inflammation evidenced by increased expressions of IL-6, IL-8 and reduced expression of IL-10. MIRI significantly increased cell apoptosis in the lung as increased levels of apoptotosis, Bax, cleaved caspase-3, and reduced expression of Bcl-2 was observed, which was concomitant with reduced p-GSK-3β. All these changes were reversed/prevented by ischemic post-conditioning, while these beneficial effects of ischemic post-conditioning were abolished by GSK-3β inhibition. Conclusion: Myocardial ischemia reperfusion injury induces acute lung injury by induction of inflammation and cell apoptosis. Ischemic post-conditioning protects the lung from ALI following MIRI by increasing p-GSK-3β. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-05-01 |
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://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502017000500376 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502017000500376 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/s0102-865020170050000007 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia |
publisher.none.fl_str_mv |
Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia |
dc.source.none.fl_str_mv |
Acta Cirúrgica Brasileira v.32 n.5 2017 reponame:Acta Cirúrgica Brasileira (Online) instname:Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC) instacron:SBDPC |
instname_str |
Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC) |
instacron_str |
SBDPC |
institution |
SBDPC |
reponame_str |
Acta Cirúrgica Brasileira (Online) |
collection |
Acta Cirúrgica Brasileira (Online) |
repository.name.fl_str_mv |
Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC) |
repository.mail.fl_str_mv |
||sgolden@terra.com.br |
_version_ |
1752126444424658944 |