Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo

Detalhes bibliográficos
Autor(a) principal: Wang,Jiyuan
Data de Publicação: 2022
Outros Autores: Chen,Yu
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=S0102-86502022000300206
Resumo: ABSTRACT Purpose: To explore the mechanism and investigate the protective effect of hydroxysafflor yellow A (HSYA) on renal oxidative stress, which cyclosporine A (CsA) induces. Methods: HK-2 cells were treated with CsA to get CsA-induced oxidative stress. The effects on oxidative stress and apoptosis of HK-2 cells were detected. The contents of SOD, MDA, GSH-Px, ROS, and CAT in serum were measured, and the expression of apoptosis-related proteins was detected by western blot. Then, established the renal oxidative stress injury rats to verify the efficacy of HSYA. Results: HSYA could reduce the ROS and MDA contents induced by CsA. Compared with the CsA group, the activities of SOD, CAT, and GSH-Px increased significantly when treated with HSYA. HSYA could inhibit CsA-induced apoptosis in HK-2 cells, and promote the protein of Bcl-2 and inhibit the expression of Bax. Animal experiments showed that HSYA could reduce CsA-induced renal cell injury by reducing glomerular cell vacuoles and inflammatory factors in tissues. It also decreased serum creatinine (Crea) and blood urea nitrogen, increased Crea clearance significantly. Conclusions: HSYA could significantly improve the antioxidant capacity of the kidney cells and inhibit cell apoptosis, thereby effectively ameliorating CsA-induced oxidative stress in vitro and in vivo.
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spelling Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivoCyclosporineOxidative StressApoptosisABSTRACT Purpose: To explore the mechanism and investigate the protective effect of hydroxysafflor yellow A (HSYA) on renal oxidative stress, which cyclosporine A (CsA) induces. Methods: HK-2 cells were treated with CsA to get CsA-induced oxidative stress. The effects on oxidative stress and apoptosis of HK-2 cells were detected. The contents of SOD, MDA, GSH-Px, ROS, and CAT in serum were measured, and the expression of apoptosis-related proteins was detected by western blot. Then, established the renal oxidative stress injury rats to verify the efficacy of HSYA. Results: HSYA could reduce the ROS and MDA contents induced by CsA. Compared with the CsA group, the activities of SOD, CAT, and GSH-Px increased significantly when treated with HSYA. HSYA could inhibit CsA-induced apoptosis in HK-2 cells, and promote the protein of Bcl-2 and inhibit the expression of Bax. Animal experiments showed that HSYA could reduce CsA-induced renal cell injury by reducing glomerular cell vacuoles and inflammatory factors in tissues. It also decreased serum creatinine (Crea) and blood urea nitrogen, increased Crea clearance significantly. Conclusions: HSYA could significantly improve the antioxidant capacity of the kidney cells and inhibit cell apoptosis, thereby effectively ameliorating CsA-induced oxidative stress in vitro and in vivo.Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia2022-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502022000300206Acta Cirúrgica Brasileira v.37 n.3 2022reponame:Acta Cirúrgica Brasileira (Online)instname:Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)instacron:SBDPC10.1590/acb370305info:eu-repo/semantics/openAccessWang,JiyuanChen,Yueng2022-06-13T00:00:00Zoai:scielo:S0102-86502022000300206Revistahttps://www.bvs-vet.org.br/vetindex/periodicos/acta-cirurgica-brasileira/https://old.scielo.br/oai/scielo-oai.php||sgolden@terra.com.br0102-86501678-2674opendoar:2022-06-13T00:00Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)false
dc.title.none.fl_str_mv Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
title Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
spellingShingle Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
Wang,Jiyuan
Cyclosporine
Oxidative Stress
Apoptosis
title_short Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
title_full Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
title_fullStr Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
title_full_unstemmed Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
title_sort Protective effect of hydroxysafflor yellow A on cyclosporin A-induced renal oxidative stress in vitro and in vivo
author Wang,Jiyuan
author_facet Wang,Jiyuan
Chen,Yu
author_role author
author2 Chen,Yu
author2_role author
dc.contributor.author.fl_str_mv Wang,Jiyuan
Chen,Yu
dc.subject.por.fl_str_mv Cyclosporine
Oxidative Stress
Apoptosis
topic Cyclosporine
Oxidative Stress
Apoptosis
description ABSTRACT Purpose: To explore the mechanism and investigate the protective effect of hydroxysafflor yellow A (HSYA) on renal oxidative stress, which cyclosporine A (CsA) induces. Methods: HK-2 cells were treated with CsA to get CsA-induced oxidative stress. The effects on oxidative stress and apoptosis of HK-2 cells were detected. The contents of SOD, MDA, GSH-Px, ROS, and CAT in serum were measured, and the expression of apoptosis-related proteins was detected by western blot. Then, established the renal oxidative stress injury rats to verify the efficacy of HSYA. Results: HSYA could reduce the ROS and MDA contents induced by CsA. Compared with the CsA group, the activities of SOD, CAT, and GSH-Px increased significantly when treated with HSYA. HSYA could inhibit CsA-induced apoptosis in HK-2 cells, and promote the protein of Bcl-2 and inhibit the expression of Bax. Animal experiments showed that HSYA could reduce CsA-induced renal cell injury by reducing glomerular cell vacuoles and inflammatory factors in tissues. It also decreased serum creatinine (Crea) and blood urea nitrogen, increased Crea clearance significantly. Conclusions: HSYA could significantly improve the antioxidant capacity of the kidney cells and inhibit cell apoptosis, thereby effectively ameliorating CsA-induced oxidative stress in vitro and in vivo.
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=S0102-86502022000300206
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dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/acb370305
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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.37 n.3 2022
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)
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repository.name.fl_str_mv Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)
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