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

被引:21
|
作者
Huang, Jianhua [1 ,2 ]
Li, Li [1 ]
Yuan, Weifeng [1 ]
Zheng, Linxin [1 ]
Guo, Zhenhui [3 ,4 ]
Huang, Wenjie [1 ,4 ]
机构
[1] Gen Hosp Guangzhou Mil Command PLA, Dept Resp Med, Guangzhou, Guangdong, Peoples R China
[2] Chenzhou 1 Peoples Hosp, Dept Pulm Med, Chenzhou, Hunan, Peoples R China
[3] Gen Hosp Guangzhou Mil Command PLA, Dept Med Intens Care Unit, Guangzhou, Guangdong, Peoples R China
[4] Guangdong Prov Key Lab Geriatr Infect & Organ Fun, Guangzhou, Guangdong, Peoples R China
关键词
ALVEOLAR-CAPILLARY BARRIER; INNATE IMMUNITY; INVOLVEMENT; CHEMOKINES; ACTIVATION; OUTCOMES; MODEL; MAPK;
D O I
10.1155/2016/7349603
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 I kappa B-alpha and NF-kappa Bp65 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-alpha and IL-1 beta secretion in BALF after LPS challenge. In conclusion, NBD protects against LPS-induced ALI in mice.
引用
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页数:11
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