Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition

Detalhes bibliográficos
Autor(a) principal: Puukila, Stephanie
Data de Publicação: 2015
Outros Autores: Bryan, Sean, Laakso, Anna, Abdel-Malak, Jessica, Gurney, Carli, Agostino, Adrian, Belló-Klein, Adriane, Prasad, Kailash, Khaper, Neelam
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/224774
Resumo: Cardiac iron overload is directly associated with cardiac dysfunction and can ultimately lead to heart failure. This study examined the effect of secoisolariciresinol diglucoside (SDG), a component of flaxseed, on iron overload induced cardiac damage by evaluating oxidative stress, inflammation and apoptosis in H9c2 cardiomyocytes. Cells were incubated with 50 μ5M iron for 24 hours and/or a 24 hour pre-treatment of 500 μ M SDG. Cardiac iron overload resulted in increased oxidative stress and gene expression of the inflammatory mediators tumor necrosis factor-α, interleukin-10 and interferon γ, as well as matrix metalloproteinases-2 and -9. Increased apoptosis was evident by increased active caspase 3/7 activity and increased protein expression of Forkhead box O3a, caspase 3 and Bax. Cardiac iron overload also resulted in increased protein expression of p70S6 Kinase 1 and decreased expression of AMP-activated protein kinase. Pre-treatment with SDG abrogated the iron-induced increases in oxidative stress, inflammation and apoptosis, as well as the increased p70S6 Kinase 1 and decreased AMP-activated protein kinase expression. The decrease in superoxide dismutase activity by iron treatment was prevented by pre-treatment with SDG in the presence of iron. Based on these findings we conclude that SDG was cytoprotective in an in vitro model of iron overload induced redox-inflammatory damage, suggesting a novel potential role for SDG in cardiac iron overload.
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spelling Puukila, StephanieBryan, SeanLaakso, AnnaAbdel-Malak, JessicaGurney, CarliAgostino, AdrianBelló-Klein, AdrianePrasad, KailashKhaper, Neelam2021-07-29T04:31:23Z20151932-6203http://hdl.handle.net/10183/224774001058162Cardiac iron overload is directly associated with cardiac dysfunction and can ultimately lead to heart failure. This study examined the effect of secoisolariciresinol diglucoside (SDG), a component of flaxseed, on iron overload induced cardiac damage by evaluating oxidative stress, inflammation and apoptosis in H9c2 cardiomyocytes. Cells were incubated with 50 μ5M iron for 24 hours and/or a 24 hour pre-treatment of 500 μ M SDG. Cardiac iron overload resulted in increased oxidative stress and gene expression of the inflammatory mediators tumor necrosis factor-α, interleukin-10 and interferon γ, as well as matrix metalloproteinases-2 and -9. Increased apoptosis was evident by increased active caspase 3/7 activity and increased protein expression of Forkhead box O3a, caspase 3 and Bax. Cardiac iron overload also resulted in increased protein expression of p70S6 Kinase 1 and decreased expression of AMP-activated protein kinase. Pre-treatment with SDG abrogated the iron-induced increases in oxidative stress, inflammation and apoptosis, as well as the increased p70S6 Kinase 1 and decreased AMP-activated protein kinase expression. The decrease in superoxide dismutase activity by iron treatment was prevented by pre-treatment with SDG in the presence of iron. Based on these findings we conclude that SDG was cytoprotective in an in vitro model of iron overload induced redox-inflammatory damage, suggesting a novel potential role for SDG in cardiac iron overload.application/pdfengPloS one. San Francisco. Vol. 10, no. 3 (Mar. 2015), e0122852, 16 f.Sobrecarga de ferroEstresse oxidativoCardiopatiasSecoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload conditionEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001058162.pdf.txt001058162.pdf.txtExtracted Texttext/plain42412http://www.lume.ufrgs.br/bitstream/10183/224774/2/001058162.pdf.txt0c5125b9885876464dc8f84094265318MD52ORIGINAL001058162.pdfTexto completo (inglês)application/pdf4851758http://www.lume.ufrgs.br/bitstream/10183/224774/1/001058162.pdfdf3ea07065b029ac35b94e10e2eb420fMD5110183/2247742023-01-20 06:01:36.865927oai:www.lume.ufrgs.br:10183/224774Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2023-01-20T08:01:36Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
title Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
spellingShingle Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
Puukila, Stephanie
Sobrecarga de ferro
Estresse oxidativo
Cardiopatias
title_short Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
title_full Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
title_fullStr Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
title_full_unstemmed Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
title_sort Secoisolariciresinol diglucoside abrogates oxidative stress-induced damage in cardiac iron overload condition
author Puukila, Stephanie
author_facet Puukila, Stephanie
Bryan, Sean
Laakso, Anna
Abdel-Malak, Jessica
Gurney, Carli
Agostino, Adrian
Belló-Klein, Adriane
Prasad, Kailash
Khaper, Neelam
author_role author
author2 Bryan, Sean
Laakso, Anna
Abdel-Malak, Jessica
Gurney, Carli
Agostino, Adrian
Belló-Klein, Adriane
Prasad, Kailash
Khaper, Neelam
author2_role author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Puukila, Stephanie
Bryan, Sean
Laakso, Anna
Abdel-Malak, Jessica
Gurney, Carli
Agostino, Adrian
Belló-Klein, Adriane
Prasad, Kailash
Khaper, Neelam
dc.subject.por.fl_str_mv Sobrecarga de ferro
Estresse oxidativo
Cardiopatias
topic Sobrecarga de ferro
Estresse oxidativo
Cardiopatias
description Cardiac iron overload is directly associated with cardiac dysfunction and can ultimately lead to heart failure. This study examined the effect of secoisolariciresinol diglucoside (SDG), a component of flaxseed, on iron overload induced cardiac damage by evaluating oxidative stress, inflammation and apoptosis in H9c2 cardiomyocytes. Cells were incubated with 50 μ5M iron for 24 hours and/or a 24 hour pre-treatment of 500 μ M SDG. Cardiac iron overload resulted in increased oxidative stress and gene expression of the inflammatory mediators tumor necrosis factor-α, interleukin-10 and interferon γ, as well as matrix metalloproteinases-2 and -9. Increased apoptosis was evident by increased active caspase 3/7 activity and increased protein expression of Forkhead box O3a, caspase 3 and Bax. Cardiac iron overload also resulted in increased protein expression of p70S6 Kinase 1 and decreased expression of AMP-activated protein kinase. Pre-treatment with SDG abrogated the iron-induced increases in oxidative stress, inflammation and apoptosis, as well as the increased p70S6 Kinase 1 and decreased AMP-activated protein kinase expression. The decrease in superoxide dismutase activity by iron treatment was prevented by pre-treatment with SDG in the presence of iron. Based on these findings we conclude that SDG was cytoprotective in an in vitro model of iron overload induced redox-inflammatory damage, suggesting a novel potential role for SDG in cardiac iron overload.
publishDate 2015
dc.date.issued.fl_str_mv 2015
dc.date.accessioned.fl_str_mv 2021-07-29T04:31:23Z
dc.type.driver.fl_str_mv Estrangeiro
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dc.identifier.uri.fl_str_mv http://hdl.handle.net/10183/224774
dc.identifier.issn.pt_BR.fl_str_mv 1932-6203
dc.identifier.nrb.pt_BR.fl_str_mv 001058162
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dc.language.iso.fl_str_mv eng
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dc.relation.ispartof.pt_BR.fl_str_mv PloS one. San Francisco. Vol. 10, no. 3 (Mar. 2015), e0122852, 16 f.
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