Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress

Abstract Purpose: To investigate the protective mechanisms of propofol (Pro) on renal ischemia/reperfusion (I/R) injury by studying its impact on renal I/R endoplasmic reticulum stress. Methods: Eighteen male Sprague-Dawley rats (SD rats) were randomly divided into three groups: the I/R group, the Pro pretreatment group, and the control group, and corresponding treatments were performed. The levels of serum creatinine (Cr) and blood urea nitrogen (BUN) of each group were detected. The expression levels of CCAAT-enhancer-binding protein (C/EBP) homology protein (CHOP) and caspase-12 protein within renal tissue samples were detected by western blot. Results: The periodic acid-Schiff (PAS) staining was performed to observe the morphological changes within the renal tissues, and the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay was performed to detect the presence of renal apoptosis. The Pro pretreatment significantly reduced the serum Cr and BUN levels, as well as the expressions levels of CHOP and caspase-12 protein inside the kidney of I/R rats, improving renal pathological injury and reducing the I/R-induced renal apoptosis. Conclusion: Propofol could downregulate the expression of stress-apoptotic proteins CHOP and caspase-12 in the endoplasmic reticulum, thus reducing renal I/R injury.

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Main Authors: Su,Mengqin, Ren,Sueng, Zhong,Wei, Han,Xueping
Format: Digital revista
Language:English
Published: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 2017
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502017000700533
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spelling oai:scielo:S0102-865020170007005332017-08-02Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stressSu,MengqinRen,SuengZhong,WeiHan,Xueping Endoplasmic Reticulum Stress Reperfusion Injury Propofol Kidney Rats Abstract Purpose: To investigate the protective mechanisms of propofol (Pro) on renal ischemia/reperfusion (I/R) injury by studying its impact on renal I/R endoplasmic reticulum stress. Methods: Eighteen male Sprague-Dawley rats (SD rats) were randomly divided into three groups: the I/R group, the Pro pretreatment group, and the control group, and corresponding treatments were performed. The levels of serum creatinine (Cr) and blood urea nitrogen (BUN) of each group were detected. The expression levels of CCAAT-enhancer-binding protein (C/EBP) homology protein (CHOP) and caspase-12 protein within renal tissue samples were detected by western blot. Results: The periodic acid-Schiff (PAS) staining was performed to observe the morphological changes within the renal tissues, and the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay was performed to detect the presence of renal apoptosis. The Pro pretreatment significantly reduced the serum Cr and BUN levels, as well as the expressions levels of CHOP and caspase-12 protein inside the kidney of I/R rats, improving renal pathological injury and reducing the I/R-induced renal apoptosis. Conclusion: Propofol could downregulate the expression of stress-apoptotic proteins CHOP and caspase-12 in the endoplasmic reticulum, thus reducing renal I/R injury.info:eu-repo/semantics/openAccessSociedade Brasileira para o Desenvolvimento da Pesquisa em CirurgiaActa Cirúrgica Brasileira v.32 n.7 20172017-07-01info:eu-repo/semantics/articletext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502017000700533en10.1590/s0102-865020170070000004
institution SCIELO
collection OJS
country Brasil
countrycode BR
component Revista
access En linea
databasecode rev-scielo-br
tag revista
region America del Sur
libraryname SciELO
language English
format Digital
author Su,Mengqin
Ren,Sueng
Zhong,Wei
Han,Xueping
spellingShingle Su,Mengqin
Ren,Sueng
Zhong,Wei
Han,Xueping
Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress
author_facet Su,Mengqin
Ren,Sueng
Zhong,Wei
Han,Xueping
author_sort Su,Mengqin
title Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress
title_short Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress
title_full Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress
title_fullStr Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress
title_full_unstemmed Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress
title_sort impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress
description Abstract Purpose: To investigate the protective mechanisms of propofol (Pro) on renal ischemia/reperfusion (I/R) injury by studying its impact on renal I/R endoplasmic reticulum stress. Methods: Eighteen male Sprague-Dawley rats (SD rats) were randomly divided into three groups: the I/R group, the Pro pretreatment group, and the control group, and corresponding treatments were performed. The levels of serum creatinine (Cr) and blood urea nitrogen (BUN) of each group were detected. The expression levels of CCAAT-enhancer-binding protein (C/EBP) homology protein (CHOP) and caspase-12 protein within renal tissue samples were detected by western blot. Results: The periodic acid-Schiff (PAS) staining was performed to observe the morphological changes within the renal tissues, and the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay was performed to detect the presence of renal apoptosis. The Pro pretreatment significantly reduced the serum Cr and BUN levels, as well as the expressions levels of CHOP and caspase-12 protein inside the kidney of I/R rats, improving renal pathological injury and reducing the I/R-induced renal apoptosis. Conclusion: Propofol could downregulate the expression of stress-apoptotic proteins CHOP and caspase-12 in the endoplasmic reticulum, thus reducing renal I/R injury.
publisher Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
publishDate 2017
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502017000700533
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AT rensueng impactofpropofolonrenalischemiareperfusionendoplasmicreticulumstress
AT zhongwei impactofpropofolonrenalischemiareperfusionendoplasmicreticulumstress
AT hanxueping impactofpropofolonrenalischemiareperfusionendoplasmicreticulumstress
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