Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Acta Cirúrgica Brasileira (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502015000600422 |
Resumo: | PURPOSE:To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway.METHODS: Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed.RESULTS: Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins.CONCLUSION:Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway. |
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Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathwayIschemiaReperfusion InjuryOxidative StressKidneyRatsPURPOSE:To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway.METHODS: Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed.RESULTS: Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins.CONCLUSION:Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway.Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia2015-06-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502015000600422Acta Cirúrgica Brasileira v.30 n.6 2015reponame:Acta Cirúrgica Brasileira (Online)instname:Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)instacron:SBDPC10.1590/S0102-865020150060000008info:eu-repo/semantics/openAccessJiang,GuanjunLiu,XiuhengWang,MinChen,HuiChen,ZhiyuanQiu,Taoeng2015-10-08T00:00:00Zoai:scielo:S0102-86502015000600422Revistahttps://www.bvs-vet.org.br/vetindex/periodicos/acta-cirurgica-brasileira/https://old.scielo.br/oai/scielo-oai.php||sgolden@terra.com.br0102-86501678-2674opendoar:2015-10-08T00:00Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)false |
dc.title.none.fl_str_mv |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway |
title |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway |
spellingShingle |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway Jiang,Guanjun Ischemia Reperfusion Injury Oxidative Stress Kidney Rats |
title_short |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway |
title_full |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway |
title_fullStr |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway |
title_full_unstemmed |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway |
title_sort |
Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway |
author |
Jiang,Guanjun |
author_facet |
Jiang,Guanjun Liu,Xiuheng Wang,Min Chen,Hui Chen,Zhiyuan Qiu,Tao |
author_role |
author |
author2 |
Liu,Xiuheng Wang,Min Chen,Hui Chen,Zhiyuan Qiu,Tao |
author2_role |
author author author author author |
dc.contributor.author.fl_str_mv |
Jiang,Guanjun Liu,Xiuheng Wang,Min Chen,Hui Chen,Zhiyuan Qiu,Tao |
dc.subject.por.fl_str_mv |
Ischemia Reperfusion Injury Oxidative Stress Kidney Rats |
topic |
Ischemia Reperfusion Injury Oxidative Stress Kidney Rats |
description |
PURPOSE:To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway.METHODS: Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed.RESULTS: Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins.CONCLUSION:Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-06-01 |
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=S0102-86502015000600422 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502015000600422 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0102-865020150060000008 |
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 para o Desenvolvimento da Pesquisa em Cirurgia |
publisher.none.fl_str_mv |
Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia |
dc.source.none.fl_str_mv |
Acta Cirúrgica Brasileira v.30 n.6 2015 reponame:Acta Cirúrgica Brasileira (Online) instname:Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC) instacron:SBDPC |
instname_str |
Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC) |
instacron_str |
SBDPC |
institution |
SBDPC |
reponame_str |
Acta Cirúrgica Brasileira (Online) |
collection |
Acta Cirúrgica Brasileira (Online) |
repository.name.fl_str_mv |
Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC) |
repository.mail.fl_str_mv |
||sgolden@terra.com.br |
_version_ |
1752126443183144960 |