NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway

The aim of the present study is to investigate the protective effects and relevant mechanisms exerted by NEMO-binding domain peptide (NBD) against lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice. The ALI model was induced by intratracheally administered atomized LPS (5 mg/kg) to B...

Full description

Saved in:
Bibliographic Details
Main Authors: Jianhua Huang, Li Li, Weifeng Yuan, Linxin Zheng, Zhenhui Guo, Wenjie Huang
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2016/7349603
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849693020911304704
author Jianhua Huang
Li Li
Weifeng Yuan
Linxin Zheng
Zhenhui Guo
Wenjie Huang
author_facet Jianhua Huang
Li Li
Weifeng Yuan
Linxin Zheng
Zhenhui Guo
Wenjie Huang
author_sort Jianhua Huang
collection DOAJ
description The aim of the present study is to investigate the protective effects and relevant mechanisms exerted by NEMO-binding domain peptide (NBD) against lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice. The ALI model was induced by intratracheally administered atomized LPS (5 mg/kg) to BABL/c mice. Half an hour before LPS administration, we treated the mice with increasing concentrations of intratracheally administered NBD or saline aerosol. Two hours after LPS administration, each group of mice was sacrificed. We observed that NBD pretreatment significantly attenuated LPS-induced lung histopathological injury in a dose-dependent manner. Western blotting established that NBD pretreatment obviously attenuated LPS-induced IκB-α and NF-κBp65 activation and NOX1, NOX2, and NOX4 overexpression. Furthermore, NBD pretreatment increased SOD and T-AOC activity and decreased MDA levels in lung tissue. In addition, NBD also inhibited TNF-α and IL-1β secretion in BALF after LPS challenge. In conclusion, NBD protects against LPS-induced ALI in mice.
format Article
id doaj-art-95ebb84d46c243a5adb9b873c2c04a64
institution DOAJ
issn 0962-9351
1466-1861
language English
publishDate 2016-01-01
publisher Wiley
record_format Article
series Mediators of Inflammation
spelling doaj-art-95ebb84d46c243a5adb9b873c2c04a642025-08-20T03:20:33ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/73496037349603NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling PathwayJianhua Huang0Li Li1Weifeng Yuan2Linxin Zheng3Zhenhui Guo4Wenjie Huang5Department of Respiratory Medicine, General Hospital of Guangzhou Military Command of PLA, Guangzhou, Guangdong, ChinaDepartment of Respiratory Medicine, General Hospital of Guangzhou Military Command of PLA, Guangzhou, Guangdong, ChinaDepartment of Respiratory Medicine, General Hospital of Guangzhou Military Command of PLA, Guangzhou, Guangdong, ChinaDepartment of Respiratory Medicine, General Hospital of Guangzhou Military Command of PLA, Guangzhou, Guangdong, ChinaDepartment of Medical Intensive Care Unit, General Hospital of Guangzhou Military Command of PLA, Guangzhou, Guangdong, ChinaDepartment of Respiratory Medicine, General Hospital of Guangzhou Military Command of PLA, Guangzhou, Guangdong, ChinaThe aim of the present study is to investigate the protective effects and relevant mechanisms exerted by NEMO-binding domain peptide (NBD) against lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice. The ALI model was induced by intratracheally administered atomized LPS (5 mg/kg) to BABL/c mice. Half an hour before LPS administration, we treated the mice with increasing concentrations of intratracheally administered NBD or saline aerosol. Two hours after LPS administration, each group of mice was sacrificed. We observed that NBD pretreatment significantly attenuated LPS-induced lung histopathological injury in a dose-dependent manner. Western blotting established that NBD pretreatment obviously attenuated LPS-induced IκB-α and NF-κBp65 activation and NOX1, NOX2, and NOX4 overexpression. Furthermore, NBD pretreatment increased SOD and T-AOC activity and decreased MDA levels in lung tissue. In addition, NBD also inhibited TNF-α and IL-1β secretion in BALF after LPS challenge. In conclusion, NBD protects against LPS-induced ALI in mice.http://dx.doi.org/10.1155/2016/7349603
spellingShingle Jianhua Huang
Li Li
Weifeng Yuan
Linxin Zheng
Zhenhui Guo
Wenjie Huang
NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway
Mediators of Inflammation
title NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway
title_full NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway
title_fullStr NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway
title_full_unstemmed NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway
title_short NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway
title_sort nemo binding domain peptide attenuates lipopolysaccharide induced acute lung injury by inhibiting the nf κb signaling pathway
url http://dx.doi.org/10.1155/2016/7349603
work_keys_str_mv AT jianhuahuang nemobindingdomainpeptideattenuateslipopolysaccharideinducedacutelunginjurybyinhibitingthenfkbsignalingpathway
AT lili nemobindingdomainpeptideattenuateslipopolysaccharideinducedacutelunginjurybyinhibitingthenfkbsignalingpathway
AT weifengyuan nemobindingdomainpeptideattenuateslipopolysaccharideinducedacutelunginjurybyinhibitingthenfkbsignalingpathway
AT linxinzheng nemobindingdomainpeptideattenuateslipopolysaccharideinducedacutelunginjurybyinhibitingthenfkbsignalingpathway
AT zhenhuiguo nemobindingdomainpeptideattenuateslipopolysaccharideinducedacutelunginjurybyinhibitingthenfkbsignalingpathway
AT wenjiehuang nemobindingdomainpeptideattenuateslipopolysaccharideinducedacutelunginjurybyinhibitingthenfkbsignalingpathway