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Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract.

Cigarette smoking is a primary risk factor for chronic obstructive pulmonary disease (COPD), as it damages epithelial cells through a variety of mechanisms. Sulforaphane (SFN) is an antioxidant agent, which exerts protective effects against cell damage by activating the nuclear factor erythroid 2 li... Full description

Journal Title: Molecular medicine reports August 2017, Vol.16(2), pp.1241-1247
Main Author: Jiao, Zongxian
Other Authors: Chang, Jiachen , Li, Jing , Nie, Dengmei , Cui, Huijuan , Guo, Dongfang
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2017.6700
Link: http://search.proquest.com/docview/1906466147/?pq-origsite=primo
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recordid: proquest1906466147
title: Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract.
format: Article
creator:
  • Jiao, Zongxian
  • Chang, Jiachen
  • Li, Jing
  • Nie, Dengmei
  • Cui, Huijuan
  • Guo, Dongfang
subjects:
  • Alveolar Epithelial Cells–Drug Effects
  • Animals–Metabolism
  • Apoptosis–Drug Effects
  • Cell Cycle–Drug Effects
  • Cell Line–Drug Effects
  • Cell Survival–Drug Effects
  • Dose-Response Relationship, Drug–Pharmacology
  • Gene Expression Regulation–Genetics
  • Isothiocyanates–Metabolism
  • Nf-E2-Related Factor 2–Pharmacology
  • Oxidative Stress–Etiology
  • Protective Agents–Metabolism
  • Pulmonary Disease, Chronic Obstructive–Pathology
  • RNA, Messenger–Genetics
  • Rats–Metabolism
  • Reactive Oxygen Species–Metabolism
  • Smoking–Adverse Effects
  • Tobacco–Adverse Effects
  • Isothiocyanates
  • Nf-E2-Related Factor 2
  • Protective Agents
  • RNA, Messenger
  • Reactive Oxygen Species
  • Sulforafan
ispartof: Molecular medicine reports, August 2017, Vol.16(2), pp.1241-1247
description: Cigarette smoking is a primary risk factor for chronic obstructive pulmonary disease (COPD), as it damages epithelial cells through a variety of mechanisms. Sulforaphane (SFN) is an antioxidant agent, which exerts protective effects against cell damage by activating the nuclear factor erythroid 2 like 2 (NFE2L2; Nrf2). The present study was undertaken to investigate the effects and underlying mechanisms of SFN in preventing cigarette smoke extract (CSE)-induced oxidative damage to RLE-6TN rat lung epithelial cells. MTT assay was used to determine the cytotoxicity of SFN and CSE. The effect of SFN and CSE on cell cycle progression, apoptosis and intracellular reactive oxygen species (ROS) levels were analyzed using flow cytometry. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to quantify mRNA and protein expression levels of Nrf2 respectively. SFN protected RLE-6TN cells from oxidative damage, potentially via increasing Nrf2 expression and reducing ROS levels. In addition, SFN attenuated G1 phase cell cycle arrest and abrogated apoptosis. Therefore, SFN protected alveolar epithelial cells against CSE-induced oxidative injury by upregulating Nrf2 expression. The results of the present study may provide theoretical support for the clinical use of SFN in patients with COPD. Key words: cigarette smoke extract, alveolar epithelial cells, sulforaphane, nuclear factor erythroid 2 like 2
language: eng
source:
identifier: E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2017.6700
fulltext: fulltext
issn:
  • 17913004
  • 1791-3004
url: Link


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titleSulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract.
creatorJiao, Zongxian ; Chang, Jiachen ; Li, Jing ; Nie, Dengmei ; Cui, Huijuan ; Guo, Dongfang
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ispartofMolecular medicine reports, August 2017, Vol.16(2), pp.1241-1247
identifierE-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2017.6700
subjectAlveolar Epithelial Cells–Drug Effects ; Animals–Metabolism ; Apoptosis–Drug Effects ; Cell Cycle–Drug Effects ; Cell Line–Drug Effects ; Cell Survival–Drug Effects ; Dose-Response Relationship, Drug–Pharmacology ; Gene Expression Regulation–Genetics ; Isothiocyanates–Metabolism ; Nf-E2-Related Factor 2–Pharmacology ; Oxidative Stress–Etiology ; Protective Agents–Metabolism ; Pulmonary Disease, Chronic Obstructive–Pathology ; RNA, Messenger–Genetics ; Rats–Metabolism ; Reactive Oxygen Species–Metabolism ; Smoking–Adverse Effects ; Tobacco–Adverse Effects ; Isothiocyanates ; Nf-E2-Related Factor 2 ; Protective Agents ; RNA, Messenger ; Reactive Oxygen Species ; Sulforafan
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descriptionCigarette smoking is a primary risk factor for chronic obstructive pulmonary disease (COPD), as it damages epithelial cells through a variety of mechanisms. Sulforaphane (SFN) is an antioxidant agent, which exerts protective effects against cell damage by activating the nuclear factor erythroid 2 like 2 (NFE2L2; Nrf2). The present study was undertaken to investigate the effects and underlying mechanisms of SFN in preventing cigarette smoke extract (CSE)-induced oxidative damage to RLE-6TN rat lung epithelial cells. MTT assay was used to determine the cytotoxicity of SFN and CSE. The effect of SFN and CSE on cell cycle progression, apoptosis and intracellular reactive oxygen species (ROS) levels were analyzed using flow cytometry. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to quantify mRNA and protein expression levels of Nrf2 respectively. SFN protected RLE-6TN cells from oxidative damage, potentially via increasing Nrf2 expression and reducing ROS levels. In addition, SFN attenuated G1 phase cell cycle arrest and abrogated apoptosis. Therefore, SFN protected alveolar epithelial cells against CSE-induced oxidative injury by upregulating Nrf2 expression. The results of the present study may provide theoretical support for the clinical use of SFN in patients with COPD. Key words: cigarette smoke extract, alveolar epithelial cells, sulforaphane, nuclear factor erythroid 2 like 2
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