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Cobalt-protoporphyrin enhances heme oxygenase 1 expression and attenuates liver ischemia/reperfusion injury by inhibiting apoptosis

The aim of the present study was to investigate the preconditioning effect and underlying mechanisms of cobalt-protoporphyrin (CoPP) in a mouse model of liver ischemia-reperfusion (I/R) injury. Mice were divided into five groups: Sham-operated (control), I/R, I/R + CoPP, I/R + CoPP and zinc-protopor... Full description

Journal Title: Molecular Medicine Reports 03/2018, Vol.17(3), pp.4567-4572
Main Author: Li, Jing
Other Authors: Wu, Bin , Teng, Dahong , Sun, Xiaoye , Li, Junjie , Li, Jiang , Zhang, Guoliang , Cai, Jinzhen
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2018.8384
Link: http://www.spandidos-publications.com/molecular medicine reports/17/3/4567
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recordid: spandido10.3892/mmr.2018.8384
title: Cobalt-protoporphyrin enhances heme oxygenase 1 expression and attenuates liver ischemia/reperfusion injury by inhibiting apoptosis
format: Article
creator:
  • Li, Jing
  • Wu, Bin
  • Teng, Dahong
  • Sun, Xiaoye
  • Li, Junjie
  • Li, Jiang
  • Zhang, Guoliang
  • Cai, Jinzhen
subjects:
  • Cobalt-Protoporphyrin
  • Heme Oxygenase-1
  • Anti-Apoptosis
ispartof: Molecular Medicine Reports, 03/2018, Vol.17(3), pp.4567-4572
description: The aim of the present study was to investigate the preconditioning effect and underlying mechanisms of cobalt-protoporphyrin (CoPP) in a mouse model of liver ischemia-reperfusion (I/R) injury. Mice were divided into five groups: Sham-operated (control), I/R, I/R + CoPP, I/R + CoPP and zinc-protoporphyrin (ZnPP) and I/R + ZnPP. Serum levels of aspartate transaminase (AST) and alanine aminotransferase (ALT) were detected using commercial kits. The expression of the pro-apoptotic protein caspase-3 was detected by immunohistochemistry and the expression levels of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and heme oxygenase 1 (HO-1) were analyzed by western blotting. Sections of liver tissue were stained with hematoxylin and eosin to observe pathologic alterations. Furthermore, hepatocyte apoptosis was detected using a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. AST and ALT levels of the CoPP preconditioned group were significantly reduced compared with the IR injury group (P
language: eng
source:
identifier: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2018.8384
fulltext: fulltext
issn:
  • 1791-2997
  • 17912997
  • 1791-3004
  • 17913004
url: Link


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titleCobalt-protoporphyrin enhances heme oxygenase 1 expression and attenuates liver ischemia/reperfusion injury by inhibiting apoptosis
creatorLi, Jing ; Wu, Bin ; Teng, Dahong ; Sun, Xiaoye ; Li, Junjie ; Li, Jiang ; Zhang, Guoliang ; Cai, Jinzhen
ispartofMolecular Medicine Reports, 03/2018, Vol.17(3), pp.4567-4572
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subjectCobalt-Protoporphyrin ; Heme Oxygenase-1 ; Anti-Apoptosis
descriptionThe aim of the present study was to investigate the preconditioning effect and underlying mechanisms of cobalt-protoporphyrin (CoPP) in a mouse model of liver ischemia-reperfusion (I/R) injury. Mice were divided into five groups: Sham-operated (control), I/R, I/R + CoPP, I/R + CoPP and zinc-protoporphyrin (ZnPP) and I/R + ZnPP. Serum levels of aspartate transaminase (AST) and alanine aminotransferase (ALT) were detected using commercial kits. The expression of the pro-apoptotic protein caspase-3 was detected by immunohistochemistry and the expression levels of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and heme oxygenase 1 (HO-1) were analyzed by western blotting. Sections of liver tissue were stained with hematoxylin and eosin to observe pathologic alterations. Furthermore, hepatocyte apoptosis was detected using a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. AST and ALT levels of the CoPP preconditioned group were significantly reduced compared with the IR injury group (P<0.05) and liver damage was attenuated. The expression levels of the pro-apoptotic protein caspase3 was inhibited and those of HO-1 and Bcl-2 were increased in the CoPP group compared with the I/R group; the opposite results were observed in the ZnPP group. Furthermore, the percentage of apoptotic cells as detected by TUNEL was significantly decreased in the CoPP group compared with the I/R group (P<0.05); these protective effects were abrogated by ZnPP. In conclusion, the results of the present study suggested that CoPP may induce HO-1 overexpression and produce anti-apoptotic effects in liver I/R injury.
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titleCobalt-protoporphyrin enhances heme oxygenase 1 expression and attenuates liver ischemia/reperfusion injury by inhibiting apoptosis
descriptionThe aim of the present study was to investigate the preconditioning effect and underlying mechanisms of cobalt-protoporphyrin (CoPP) in a mouse model of liver ischemia-reperfusion (I/R) injury. Mice were divided into five groups: Sham-operated (control), I/R, I/R + CoPP, I/R + CoPP and zinc-protoporphyrin (ZnPP) and I/R + ZnPP. Serum levels of aspartate transaminase (AST) and alanine aminotransferase (ALT) were detected using commercial kits. The expression of the pro-apoptotic protein caspase-3 was detected by immunohistochemistry and the expression levels of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and heme oxygenase 1 (HO-1) were analyzed by western blotting. Sections of liver tissue were stained with hematoxylin and eosin to observe pathologic alterations. Furthermore, hepatocyte apoptosis was detected using a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. AST and ALT levels of the CoPP preconditioned group were significantly reduced compared with the IR injury group (P<0.05) and liver damage was attenuated. The expression levels of the pro-apoptotic protein caspase3 was inhibited and those of HO-1 and Bcl-2 were increased in the CoPP group compared with the I/R group; the opposite results were observed in the ZnPP group. Furthermore, the percentage of apoptotic cells as detected by TUNEL was significantly decreased in the CoPP group compared with the I/R group (P<0.05); these protective effects were abrogated by ZnPP. In conclusion, the results of the present study suggested that CoPP may induce HO-1 overexpression and produce anti-apoptotic effects in liver I/R injury.
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abstractThe aim of the present study was to investigate the preconditioning effect and underlying mechanisms of cobalt-protoporphyrin (CoPP) in a mouse model of liver ischemia-reperfusion (I/R) injury. Mice were divided into five groups: Sham-operated (control), I/R, I/R + CoPP, I/R + CoPP and zinc-protoporphyrin (ZnPP) and I/R + ZnPP. Serum levels of aspartate transaminase (AST) and alanine aminotransferase (ALT) were detected using commercial kits. The expression of the pro-apoptotic protein caspase-3 was detected by immunohistochemistry and the expression levels of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and heme oxygenase 1 (HO-1) were analyzed by western blotting. Sections of liver tissue were stained with hematoxylin and eosin to observe pathologic alterations. Furthermore, hepatocyte apoptosis was detected using a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. AST and ALT levels of the CoPP preconditioned group were significantly reduced compared with the IR injury group (P<0.05) and liver damage was attenuated. The expression levels of the pro-apoptotic protein caspase3 was inhibited and those of HO-1 and Bcl-2 were increased in the CoPP group compared with the I/R group; the opposite results were observed in the ZnPP group. Furthermore, the percentage of apoptotic cells as detected by TUNEL was significantly decreased in the CoPP group compared with the I/R group (P<0.05); these protective effects were abrogated by ZnPP. In conclusion, the results of the present study suggested that CoPP may induce HO-1 overexpression and produce anti-apoptotic effects in liver I/R injury.
pubD.A. Spandidos
doi10.3892/mmr.2018.8384
date2018-03