Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Food Science and Technology (Campinas) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100773 |
Resumo: | Abstract In our study, CCK-8 assay and LDH release detection were performed to detect the optimal protective concentration of GSH on HL7702 cell viability during H/R injury. HL7702 cells were randomly divided into four groups: Control group, H/R group, H/R+GSH group, and H/R+GSH+HO-1-siRNA group. Then, reactive oxygen species (ROS) was evaluated by DHE staning, MDA, T-SOD measurements; Cell injury was detected by CCK-8, LDH release, and supernatant AST and ALT levels; Apoptosis was determined by Hoechst staining and caspase 3 level. Compared with controls, H/R caused significant HL7702 cell injury evidenced as reduced cell viability, increased LDH release and apoptotic cell death (P < 0.01), with concomitant increases in ROS and MDA production (P < 0.01), while treated with GSH in H/R group significantly attenuated oxidative injury, enhanced cell viability and downregulated cell apoptosis (P < 0.01) together with HO-1 upregulation (P < 0.01). Knockdown HO-1 by its siRNA cancelled the protective effects of GSH from H/R compared with GSH group (P < 0.01). HO-1 was induced in HL7702 exposed to H/R injury and its level was obviously overexpressed after H/R injury with GSH treatment, suggesting its protective potential in GSH against H/R injury. GSH increases the expression of HO-1, which enhanced the early antioxidative activity and played a protective role against HL7702 cells H/R injury. |
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Food Science and Technology (Campinas) |
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Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signalingglutathionehepatocellularhypoxia/reoxygenation injuryHO-1Abstract In our study, CCK-8 assay and LDH release detection were performed to detect the optimal protective concentration of GSH on HL7702 cell viability during H/R injury. HL7702 cells were randomly divided into four groups: Control group, H/R group, H/R+GSH group, and H/R+GSH+HO-1-siRNA group. Then, reactive oxygen species (ROS) was evaluated by DHE staning, MDA, T-SOD measurements; Cell injury was detected by CCK-8, LDH release, and supernatant AST and ALT levels; Apoptosis was determined by Hoechst staining and caspase 3 level. Compared with controls, H/R caused significant HL7702 cell injury evidenced as reduced cell viability, increased LDH release and apoptotic cell death (P < 0.01), with concomitant increases in ROS and MDA production (P < 0.01), while treated with GSH in H/R group significantly attenuated oxidative injury, enhanced cell viability and downregulated cell apoptosis (P < 0.01) together with HO-1 upregulation (P < 0.01). Knockdown HO-1 by its siRNA cancelled the protective effects of GSH from H/R compared with GSH group (P < 0.01). HO-1 was induced in HL7702 exposed to H/R injury and its level was obviously overexpressed after H/R injury with GSH treatment, suggesting its protective potential in GSH against H/R injury. GSH increases the expression of HO-1, which enhanced the early antioxidative activity and played a protective role against HL7702 cells H/R injury.Sociedade Brasileira de Ciência e Tecnologia de Alimentos2022-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100773Food Science and Technology v.42 2022reponame:Food Science and Technology (Campinas)instname:Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA)instacron:SBCTA10.1590/fst.61221info:eu-repo/semantics/openAccessCHEN,WuyeLI,KunpingZHU,ShaomeiLUO,XiaozaiWANG,YihongLIU,ZhengyuFANG,YongpingXIA,Zhengyuaneng2022-02-22T00:00:00Zoai:scielo:S0101-20612022000100773Revistahttp://www.scielo.br/ctaONGhttps://old.scielo.br/oai/scielo-oai.php||revista@sbcta.org.br1678-457X0101-2061opendoar:2022-02-22T00:00Food Science and Technology (Campinas) - Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA)false |
dc.title.none.fl_str_mv |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling |
title |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling |
spellingShingle |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling CHEN,Wuye glutathione hepatocellular hypoxia/reoxygenation injury HO-1 |
title_short |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling |
title_full |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling |
title_fullStr |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling |
title_full_unstemmed |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling |
title_sort |
Glutathione ameliorates Hypoxia/Reoxygenation (H/R) induced hepatocyte oxidative damage via regulating HO-1 signaling |
author |
CHEN,Wuye |
author_facet |
CHEN,Wuye LI,Kunping ZHU,Shaomei LUO,Xiaozai WANG,Yihong LIU,Zhengyu FANG,Yongping XIA,Zhengyuan |
author_role |
author |
author2 |
LI,Kunping ZHU,Shaomei LUO,Xiaozai WANG,Yihong LIU,Zhengyu FANG,Yongping XIA,Zhengyuan |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
CHEN,Wuye LI,Kunping ZHU,Shaomei LUO,Xiaozai WANG,Yihong LIU,Zhengyu FANG,Yongping XIA,Zhengyuan |
dc.subject.por.fl_str_mv |
glutathione hepatocellular hypoxia/reoxygenation injury HO-1 |
topic |
glutathione hepatocellular hypoxia/reoxygenation injury HO-1 |
description |
Abstract In our study, CCK-8 assay and LDH release detection were performed to detect the optimal protective concentration of GSH on HL7702 cell viability during H/R injury. HL7702 cells were randomly divided into four groups: Control group, H/R group, H/R+GSH group, and H/R+GSH+HO-1-siRNA group. Then, reactive oxygen species (ROS) was evaluated by DHE staning, MDA, T-SOD measurements; Cell injury was detected by CCK-8, LDH release, and supernatant AST and ALT levels; Apoptosis was determined by Hoechst staining and caspase 3 level. Compared with controls, H/R caused significant HL7702 cell injury evidenced as reduced cell viability, increased LDH release and apoptotic cell death (P < 0.01), with concomitant increases in ROS and MDA production (P < 0.01), while treated with GSH in H/R group significantly attenuated oxidative injury, enhanced cell viability and downregulated cell apoptosis (P < 0.01) together with HO-1 upregulation (P < 0.01). Knockdown HO-1 by its siRNA cancelled the protective effects of GSH from H/R compared with GSH group (P < 0.01). HO-1 was induced in HL7702 exposed to H/R injury and its level was obviously overexpressed after H/R injury with GSH treatment, suggesting its protective potential in GSH against H/R injury. GSH increases the expression of HO-1, which enhanced the early antioxidative activity and played a protective role against HL7702 cells H/R injury. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-01-01 |
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=S0101-20612022000100773 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100773 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/fst.61221 |
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 Ciência e Tecnologia de Alimentos |
publisher.none.fl_str_mv |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos |
dc.source.none.fl_str_mv |
Food Science and Technology v.42 2022 reponame:Food Science and Technology (Campinas) instname:Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) instacron:SBCTA |
instname_str |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) |
instacron_str |
SBCTA |
institution |
SBCTA |
reponame_str |
Food Science and Technology (Campinas) |
collection |
Food Science and Technology (Campinas) |
repository.name.fl_str_mv |
Food Science and Technology (Campinas) - Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) |
repository.mail.fl_str_mv |
||revista@sbcta.org.br |
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1752126332871901184 |