The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress

Detalhes bibliográficos
Autor(a) principal: Sun,Chuang
Data de Publicação: 2022
Outros Autores: Wang,Tingting, Wang,Changying, Zhu,Zhenyin, Wang,Xiaoni, Xu,Jia, ,HuixiAn
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=S0102-76382022000300335
Resumo: Abstract Introduction: The objective of this study is to investigate the protective effect of kaempferol against ischemia/reperfusion (IR) injury and the underlying molecular mechanisms. Methods: H9C2 cells were pretreated with kaempferol for 24 hours and further insulted with IR injury. Cell vitality, reactive oxygen species (ROS) level, glutathione (GSH) level, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and sirtuin-3 (SIRT3), B-cell lymphoma 2 (Bcl2), and Bcl2-associated X protein (Bax) expressions were evaluated. Moreover, short interfering ribonucleic acid targeting SIRT3 was used to investigate the role of SIRT3 against IR mediated by kaempferol in vitro. IR mice models were also established to confirm the protective effects of kaempferol on IR in vivo. Results: After IR injury, H9C2 cells vitality was reduced, ROS levels, NADPH oxidase activity, and Bax expressions were increased, and GSH levels and Bcl2 expressions were decreased. After kaempferol pretreatment, the vitality of H9C2 cells was increased. The levels of ROS, NADPH oxidase activity, and Bax expression were decreased. In addition, levels of GSH and Bcl2 expression were enhanced. Furthermore, silencing SIRT3 attenuated the protective effect mediated by kaempferol, with increased ROS levels, NADPH oxidase activity, and Bax expression, along with reduced GSH level and Bcl2 expression. In vivo IR model showed that kaempferol could preserve IR-damaged cardiac function. Conclusion: Kaempferol has the capability of attenuating H9C2 cells IR injury through activating SIRT3 to inhibit oxidative stress.
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spelling The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative StressKaempferolsReperfusion InjurySirtuin-3Oxidative Stress.Abstract Introduction: The objective of this study is to investigate the protective effect of kaempferol against ischemia/reperfusion (IR) injury and the underlying molecular mechanisms. Methods: H9C2 cells were pretreated with kaempferol for 24 hours and further insulted with IR injury. Cell vitality, reactive oxygen species (ROS) level, glutathione (GSH) level, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and sirtuin-3 (SIRT3), B-cell lymphoma 2 (Bcl2), and Bcl2-associated X protein (Bax) expressions were evaluated. Moreover, short interfering ribonucleic acid targeting SIRT3 was used to investigate the role of SIRT3 against IR mediated by kaempferol in vitro. IR mice models were also established to confirm the protective effects of kaempferol on IR in vivo. Results: After IR injury, H9C2 cells vitality was reduced, ROS levels, NADPH oxidase activity, and Bax expressions were increased, and GSH levels and Bcl2 expressions were decreased. After kaempferol pretreatment, the vitality of H9C2 cells was increased. The levels of ROS, NADPH oxidase activity, and Bax expression were decreased. In addition, levels of GSH and Bcl2 expression were enhanced. Furthermore, silencing SIRT3 attenuated the protective effect mediated by kaempferol, with increased ROS levels, NADPH oxidase activity, and Bax expression, along with reduced GSH level and Bcl2 expression. In vivo IR model showed that kaempferol could preserve IR-damaged cardiac function. Conclusion: Kaempferol has the capability of attenuating H9C2 cells IR injury through activating SIRT3 to inhibit oxidative stress.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=S0102-76382022000300335Brazilian Journal of Cardiovascular Surgery v.37 n.3 2022reponame:Brazilian Journal of Cardiovascular Surgery (Online)instname:Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)instacron:SBCCV10.21470/1678-9741-2020-0549info:eu-repo/semantics/openAccessSun,ChuangWang,TingtingWang,ChangyingZhu,ZhenyinWang,XiaoniXu,Jia,HuixiAneng2022-05-31T00:00:00Zoai:scielo:S0102-76382022000300335Revistahttp://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 The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
title The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
spellingShingle The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
Sun,Chuang
Kaempferols
Reperfusion Injury
Sirtuin-3
Oxidative Stress.
title_short The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
title_full The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
title_fullStr The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
title_full_unstemmed The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
title_sort The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress
author Sun,Chuang
author_facet Sun,Chuang
Wang,Tingting
Wang,Changying
Zhu,Zhenyin
Wang,Xiaoni
Xu,Jia
,HuixiAn
author_role author
author2 Wang,Tingting
Wang,Changying
Zhu,Zhenyin
Wang,Xiaoni
Xu,Jia
,HuixiAn
author2_role author
author
author
author
author
author
dc.contributor.author.fl_str_mv Sun,Chuang
Wang,Tingting
Wang,Changying
Zhu,Zhenyin
Wang,Xiaoni
Xu,Jia
,HuixiAn
dc.subject.por.fl_str_mv Kaempferols
Reperfusion Injury
Sirtuin-3
Oxidative Stress.
topic Kaempferols
Reperfusion Injury
Sirtuin-3
Oxidative Stress.
description Abstract Introduction: The objective of this study is to investigate the protective effect of kaempferol against ischemia/reperfusion (IR) injury and the underlying molecular mechanisms. Methods: H9C2 cells were pretreated with kaempferol for 24 hours and further insulted with IR injury. Cell vitality, reactive oxygen species (ROS) level, glutathione (GSH) level, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and sirtuin-3 (SIRT3), B-cell lymphoma 2 (Bcl2), and Bcl2-associated X protein (Bax) expressions were evaluated. Moreover, short interfering ribonucleic acid targeting SIRT3 was used to investigate the role of SIRT3 against IR mediated by kaempferol in vitro. IR mice models were also established to confirm the protective effects of kaempferol on IR in vivo. Results: After IR injury, H9C2 cells vitality was reduced, ROS levels, NADPH oxidase activity, and Bax expressions were increased, and GSH levels and Bcl2 expressions were decreased. After kaempferol pretreatment, the vitality of H9C2 cells was increased. The levels of ROS, NADPH oxidase activity, and Bax expression were decreased. In addition, levels of GSH and Bcl2 expression were enhanced. Furthermore, silencing SIRT3 attenuated the protective effect mediated by kaempferol, with increased ROS levels, NADPH oxidase activity, and Bax expression, along with reduced GSH level and Bcl2 expression. In vivo IR model showed that kaempferol could preserve IR-damaged cardiac function. Conclusion: Kaempferol has the capability of attenuating H9C2 cells IR injury through activating SIRT3 to inhibit oxidative stress.
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=S0102-76382022000300335
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000300335
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.21470/1678-9741-2020-0549
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
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