Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Cardiovascular Surgery (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000300370 |
Resumo: | ABSTRACT Introduction: The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reperfusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1α (HIF-1α). Methods: Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1α was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro-inflammatory factors were measured. In addition, HIF-1α expression was assessed by immunohistochemistry and western blot analysis. Results: Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1α expression. Moreover, Dex + LV-HIF-1α reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion: Our study has made it clear that Dex inhibited the upregulation of HIF-1α in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response. |
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Brazilian Journal of Cardiovascular Surgery (Online) |
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Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1αDexmedetomidineAcute Lung InjuryDiabetesMyocardial Ischemia ReperfusionHypoxia-Inducible Factor 1Up-RegulationABSTRACT Introduction: The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reperfusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1α (HIF-1α). Methods: Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1α was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro-inflammatory factors were measured. In addition, HIF-1α expression was assessed by immunohistochemistry and western blot analysis. Results: Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1α expression. Moreover, Dex + LV-HIF-1α reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion: Our study has made it clear that Dex inhibited the upregulation of HIF-1α in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response.Sociedade Brasileira de Cirurgia Cardiovascular2022-06-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000300370Brazilian Journal of Cardiovascular Surgery v.37 n.3 2022reponame:Brazilian Journal of Cardiovascular Surgery (Online)instname:Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)instacron:SBCCV10.21470/1678-9741-2020-0591info:eu-repo/semantics/openAccessChen,SiyuWu,JianjiangYang,LongTailaiti,TaiwanguZou,TiantianHuan,YidanWang,Jiangeng2022-05-31T00:00:00Zoai:scielo:S0102-76382022000300370Revistahttp://www.rbccv.org.br/https://old.scielo.br/oai/scielo-oai.php||rosangela.monteiro@incor.usp.br|| domingo@braile.com.br|| brandau@braile.com.br1678-97410102-7638opendoar:2022-05-31T00:00Brazilian Journal of Cardiovascular Surgery (Online) - Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)false |
dc.title.none.fl_str_mv |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α |
title |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α |
spellingShingle |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α Chen,Siyu Dexmedetomidine Acute Lung Injury Diabetes Myocardial Ischemia Reperfusion Hypoxia-Inducible Factor 1 Up-Regulation |
title_short |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α |
title_full |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α |
title_fullStr |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α |
title_full_unstemmed |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α |
title_sort |
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α |
author |
Chen,Siyu |
author_facet |
Chen,Siyu Wu,Jianjiang Yang,Long Tailaiti,Taiwangu Zou,Tiantian Huan,Yidan Wang,Jiang |
author_role |
author |
author2 |
Wu,Jianjiang Yang,Long Tailaiti,Taiwangu Zou,Tiantian Huan,Yidan Wang,Jiang |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Chen,Siyu Wu,Jianjiang Yang,Long Tailaiti,Taiwangu Zou,Tiantian Huan,Yidan Wang,Jiang |
dc.subject.por.fl_str_mv |
Dexmedetomidine Acute Lung Injury Diabetes Myocardial Ischemia Reperfusion Hypoxia-Inducible Factor 1 Up-Regulation |
topic |
Dexmedetomidine Acute Lung Injury Diabetes Myocardial Ischemia Reperfusion Hypoxia-Inducible Factor 1 Up-Regulation |
description |
ABSTRACT Introduction: The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reperfusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1α (HIF-1α). Methods: Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1α was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro-inflammatory factors were measured. In addition, HIF-1α expression was assessed by immunohistochemistry and western blot analysis. Results: Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1α expression. Moreover, Dex + LV-HIF-1α reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion: Our study has made it clear that Dex inhibited the upregulation of HIF-1α in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-06-01 |
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=S0102-76382022000300370 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000300370 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.21470/1678-9741-2020-0591 |
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 de Cirurgia Cardiovascular |
publisher.none.fl_str_mv |
Sociedade Brasileira de Cirurgia Cardiovascular |
dc.source.none.fl_str_mv |
Brazilian Journal of Cardiovascular Surgery v.37 n.3 2022 reponame:Brazilian Journal of Cardiovascular Surgery (Online) instname:Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV) instacron:SBCCV |
instname_str |
Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV) |
instacron_str |
SBCCV |
institution |
SBCCV |
reponame_str |
Brazilian Journal of Cardiovascular Surgery (Online) |
collection |
Brazilian Journal of Cardiovascular Surgery (Online) |
repository.name.fl_str_mv |
Brazilian Journal of Cardiovascular Surgery (Online) - Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV) |
repository.mail.fl_str_mv |
||rosangela.monteiro@incor.usp.br|| domingo@braile.com.br|| brandau@braile.com.br |
_version_ |
1752126603201085440 |