Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts

Autores
Fernandes, Rafael O.; Bonetto, Jéssica H. P.; Baregzay, Boran; de Castro, Alexandre L.; Puukila, Stephanie; Forsyth, Heidi; Schenkel, Paulo C.; Llesuy, Susana Francisca; Brum, Ilma Simoni; Araujo, Alex Sander R.; Khaper, Neelam; Belló Klein, Adriane
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Sulforaphane is a naturally occurring isothiocyanate capable of stimulating cellular antioxidant defenses and inducing phase 2 detoxifying enzymes, which can protect cells against oxidative damage. Oxidative stress and apoptosis are intimately involved in the pathophysiology of cardiac diseases. Although sulforaphane is known for its anticancer benefits, its role in cardiac cells is just emerging. The aim of the present study was to investigate whether sulforaphane can modulate oxidative stress, apoptosis, and correlate with PGC-1α, a transcriptional cofactor involved in energy metabolism. H9c2 cardiac myoblasts were incubated with R-sulforaphane 5 µmol/L for 24 h. Cell viability, ANP gene expression, oxidative stress and apoptosis markers, and protein expression of PGC-1α were studied. In cells treated with sulforaphane, cellular viability increased (12 %) and ANP gene expression decreased (46 %) compared to control cells. Moreover, sulforaphane induced a significant increase in superoxide dismutase (103 %), catalase (101 %), and glutathione S-transferase (72 %) activity, reduced reactive oxygen species levels (15 %) and lipid peroxidation (65 %), as well as stimulated the expression of the cytoprotective enzyme heme oxygenase-1 (4-fold). Sulforaphane also promoted an increase in the expression of the anti-apoptotic protein Bcl-2 (60 %), decreasing the Bax/Bcl-2 ratio. Active Caspase 3\7 and p-JNK/JNK were also reduced by sulforaphane, suggesting a reduction in apoptotic signaling. This was associated with an increased protein expression of PGC-1α (42 %). These results suggest that sulforaphane offers cytoprotection to cardiac cells by activating PGC1-α, reducing oxidative stress, and decreasing apoptosis signaling.
Fil: Fernandes, Rafael O.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Bonetto, Jéssica H. P.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Baregzay, Boran. Lakehead University; Canadá
Fil: de Castro, Alexandre L.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Puukila, Stephanie. Lakehead University; Canadá
Fil: Forsyth, Heidi. Lakehead University; Canadá
Fil: Schenkel, Paulo C.. Universidade Federal de Pelotas; Brasil
Fil: Llesuy, Susana Francisca. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Brum, Ilma Simoni. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Araujo, Alex Sander R.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Khaper, Neelam. Lakehead University; Canadá
Fil: Belló Klein, Adriane. Universidade Federal do Rio Grande do Sul; Brasil
Materia
Oxidative Stress
Heme Oxygenase-1
Pgc-1 Alpha
Bcl-2
Caspase
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/39274
Acceder
id CONICETDig_8045f608f8e2133a29663a3dc2e551a4
oai_identifier_str oai:ri.conicet.gov.ar:11336/39274
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblastsFernandes, Rafael O.Bonetto, Jéssica H. P.Baregzay, Borande Castro, Alexandre L.Puukila, StephanieForsyth, HeidiSchenkel, Paulo C.Llesuy, Susana FranciscaBrum, Ilma SimoniAraujo, Alex Sander R.Khaper, NeelamBelló Klein, AdrianeOxidative StressHeme Oxygenase-1Pgc-1 AlphaBcl-2Caspasehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Sulforaphane is a naturally occurring isothiocyanate capable of stimulating cellular antioxidant defenses and inducing phase 2 detoxifying enzymes, which can protect cells against oxidative damage. Oxidative stress and apoptosis are intimately involved in the pathophysiology of cardiac diseases. Although sulforaphane is known for its anticancer benefits, its role in cardiac cells is just emerging. The aim of the present study was to investigate whether sulforaphane can modulate oxidative stress, apoptosis, and correlate with PGC-1α, a transcriptional cofactor involved in energy metabolism. H9c2 cardiac myoblasts were incubated with R-sulforaphane 5 µmol/L for 24 h. Cell viability, ANP gene expression, oxidative stress and apoptosis markers, and protein expression of PGC-1α were studied. In cells treated with sulforaphane, cellular viability increased (12 %) and ANP gene expression decreased (46 %) compared to control cells. Moreover, sulforaphane induced a significant increase in superoxide dismutase (103 %), catalase (101 %), and glutathione S-transferase (72 %) activity, reduced reactive oxygen species levels (15 %) and lipid peroxidation (65 %), as well as stimulated the expression of the cytoprotective enzyme heme oxygenase-1 (4-fold). Sulforaphane also promoted an increase in the expression of the anti-apoptotic protein Bcl-2 (60 %), decreasing the Bax/Bcl-2 ratio. Active Caspase 3\7 and p-JNK/JNK were also reduced by sulforaphane, suggesting a reduction in apoptotic signaling. This was associated with an increased protein expression of PGC-1α (42 %). These results suggest that sulforaphane offers cytoprotection to cardiac cells by activating PGC1-α, reducing oxidative stress, and decreasing apoptosis signaling.Fil: Fernandes, Rafael O.. Universidade Federal do Rio Grande do Sul; BrasilFil: Bonetto, Jéssica H. P.. Universidade Federal do Rio Grande do Sul; BrasilFil: Baregzay, Boran. Lakehead University; CanadáFil: de Castro, Alexandre L.. Universidade Federal do Rio Grande do Sul; BrasilFil: Puukila, Stephanie. Lakehead University; CanadáFil: Forsyth, Heidi. Lakehead University; CanadáFil: Schenkel, Paulo C.. Universidade Federal de Pelotas; BrasilFil: Llesuy, Susana Francisca. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Brum, Ilma Simoni. Universidade Federal do Rio Grande do Sul; BrasilFil: Araujo, Alex Sander R.. Universidade Federal do Rio Grande do Sul; BrasilFil: Khaper, Neelam. Lakehead University; CanadáFil: Belló Klein, Adriane. Universidade Federal do Rio Grande do Sul; BrasilSpringer2015-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/39274Fernandes, Rafael O.; Bonetto, Jéssica H. P.; Baregzay, Boran; de Castro, Alexandre L.; Puukila, Stephanie; et al.; Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts; Springer; Molecular and Cellular Biochemistry; 401; 1-2; 3-2015; 61-700300-8177CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/ 10.1007/s11010-014-2292-zinfo:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-014-2292-zinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:12:25Zoai:ri.conicet.gov.ar:11336/39274instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:12:25.6CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
title Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
spellingShingle Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
Fernandes, Rafael O.
Oxidative Stress
Heme Oxygenase-1
Pgc-1 Alpha
Bcl-2
Caspase
title_short Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
title_full Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
title_fullStr Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
title_full_unstemmed Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
title_sort Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts
dc.creator.none.fl_str_mv Fernandes, Rafael O.
Bonetto, Jéssica H. P.
Baregzay, Boran
de Castro, Alexandre L.
Puukila, Stephanie
Forsyth, Heidi
Schenkel, Paulo C.
Llesuy, Susana Francisca
Brum, Ilma Simoni
Araujo, Alex Sander R.
Khaper, Neelam
Belló Klein, Adriane
author Fernandes, Rafael O.
author_facet Fernandes, Rafael O.
Bonetto, Jéssica H. P.
Baregzay, Boran
de Castro, Alexandre L.
Puukila, Stephanie
Forsyth, Heidi
Schenkel, Paulo C.
Llesuy, Susana Francisca
Brum, Ilma Simoni
Araujo, Alex Sander R.
Khaper, Neelam
Belló Klein, Adriane
author_role author
author2 Bonetto, Jéssica H. P.
Baregzay, Boran
de Castro, Alexandre L.
Puukila, Stephanie
Forsyth, Heidi
Schenkel, Paulo C.
Llesuy, Susana Francisca
Brum, Ilma Simoni
Araujo, Alex Sander R.
Khaper, Neelam
Belló Klein, Adriane
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Oxidative Stress
Heme Oxygenase-1
Pgc-1 Alpha
Bcl-2
Caspase
topic Oxidative Stress
Heme Oxygenase-1
Pgc-1 Alpha
Bcl-2
Caspase
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Sulforaphane is a naturally occurring isothiocyanate capable of stimulating cellular antioxidant defenses and inducing phase 2 detoxifying enzymes, which can protect cells against oxidative damage. Oxidative stress and apoptosis are intimately involved in the pathophysiology of cardiac diseases. Although sulforaphane is known for its anticancer benefits, its role in cardiac cells is just emerging. The aim of the present study was to investigate whether sulforaphane can modulate oxidative stress, apoptosis, and correlate with PGC-1α, a transcriptional cofactor involved in energy metabolism. H9c2 cardiac myoblasts were incubated with R-sulforaphane 5 µmol/L for 24 h. Cell viability, ANP gene expression, oxidative stress and apoptosis markers, and protein expression of PGC-1α were studied. In cells treated with sulforaphane, cellular viability increased (12 %) and ANP gene expression decreased (46 %) compared to control cells. Moreover, sulforaphane induced a significant increase in superoxide dismutase (103 %), catalase (101 %), and glutathione S-transferase (72 %) activity, reduced reactive oxygen species levels (15 %) and lipid peroxidation (65 %), as well as stimulated the expression of the cytoprotective enzyme heme oxygenase-1 (4-fold). Sulforaphane also promoted an increase in the expression of the anti-apoptotic protein Bcl-2 (60 %), decreasing the Bax/Bcl-2 ratio. Active Caspase 3\7 and p-JNK/JNK were also reduced by sulforaphane, suggesting a reduction in apoptotic signaling. This was associated with an increased protein expression of PGC-1α (42 %). These results suggest that sulforaphane offers cytoprotection to cardiac cells by activating PGC1-α, reducing oxidative stress, and decreasing apoptosis signaling.
Fil: Fernandes, Rafael O.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Bonetto, Jéssica H. P.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Baregzay, Boran. Lakehead University; Canadá
Fil: de Castro, Alexandre L.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Puukila, Stephanie. Lakehead University; Canadá
Fil: Forsyth, Heidi. Lakehead University; Canadá
Fil: Schenkel, Paulo C.. Universidade Federal de Pelotas; Brasil
Fil: Llesuy, Susana Francisca. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Brum, Ilma Simoni. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Araujo, Alex Sander R.. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Khaper, Neelam. Lakehead University; Canadá
Fil: Belló Klein, Adriane. Universidade Federal do Rio Grande do Sul; Brasil
description Sulforaphane is a naturally occurring isothiocyanate capable of stimulating cellular antioxidant defenses and inducing phase 2 detoxifying enzymes, which can protect cells against oxidative damage. Oxidative stress and apoptosis are intimately involved in the pathophysiology of cardiac diseases. Although sulforaphane is known for its anticancer benefits, its role in cardiac cells is just emerging. The aim of the present study was to investigate whether sulforaphane can modulate oxidative stress, apoptosis, and correlate with PGC-1α, a transcriptional cofactor involved in energy metabolism. H9c2 cardiac myoblasts were incubated with R-sulforaphane 5 µmol/L for 24 h. Cell viability, ANP gene expression, oxidative stress and apoptosis markers, and protein expression of PGC-1α were studied. In cells treated with sulforaphane, cellular viability increased (12 %) and ANP gene expression decreased (46 %) compared to control cells. Moreover, sulforaphane induced a significant increase in superoxide dismutase (103 %), catalase (101 %), and glutathione S-transferase (72 %) activity, reduced reactive oxygen species levels (15 %) and lipid peroxidation (65 %), as well as stimulated the expression of the cytoprotective enzyme heme oxygenase-1 (4-fold). Sulforaphane also promoted an increase in the expression of the anti-apoptotic protein Bcl-2 (60 %), decreasing the Bax/Bcl-2 ratio. Active Caspase 3\7 and p-JNK/JNK were also reduced by sulforaphane, suggesting a reduction in apoptotic signaling. This was associated with an increased protein expression of PGC-1α (42 %). These results suggest that sulforaphane offers cytoprotection to cardiac cells by activating PGC1-α, reducing oxidative stress, and decreasing apoptosis signaling.
publishDate 2015
dc.date.none.fl_str_mv 2015-03
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/39274
Fernandes, Rafael O.; Bonetto, Jéssica H. P.; Baregzay, Boran; de Castro, Alexandre L.; Puukila, Stephanie; et al.; Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts; Springer; Molecular and Cellular Biochemistry; 401; 1-2; 3-2015; 61-70
0300-8177
CONICET Digital
CONICET
url http://hdl.handle.net/11336/39274
identifier_str_mv Fernandes, Rafael O.; Bonetto, Jéssica H. P.; Baregzay, Boran; de Castro, Alexandre L.; Puukila, Stephanie; et al.; Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts; Springer; Molecular and Cellular Biochemistry; 401; 1-2; 3-2015; 61-70
0300-8177
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/ 10.1007/s11010-014-2292-z
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-014-2292-z
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 12.982451

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