Cigarette smoke enhances β-defensin 2 expression in rat airways via nuclear factor-κB activation

被引：46

作者：

Chen, L. ^{[1
,2
]}

Sun, B-B. ^{[1
,2
]}

Wang, T. ^{[1
,2
]}

Wang, X. ^{[1
,2
]}

Li, J-Q. ^{[1
,2
]}

Wang, H-X. ^{[1
,2
]}

Zhang, S-F. ^{[3
]}

Liu, D-S. ^{[1
,2
]}

Liu, L. ^{[2
,4
]}

Xu, D. ^{[1
,2
]}

Ou, X-M. ^{[1
,2
]}

Chen, Y-J. ^{[1
,2
]}

Yang, T. ^{[1
,2
]}

Zhou, H. ^{[1
,2
]}

Wen, F-Q. ^{[1
,2
]}

机构：

[1] Sichuan Univ, Div Pulm Dis, State Key Lab Biotherapy China, W China Hosp,W China Sch Med, Chengdu 610041, Sichuan, Peoples R China

[2] Sichuan Univ, Dept Resp Med, W China Hosp, W China Sch Med, Chengdu 610041, Sichuan, Peoples R China

[3] Sichuan Univ, Dept Pathol, W China Hosp, W China Sch Med, Chengdu 610041, Sichuan, Peoples R China

[4] Third Peoples Hosp Mianyang, Dept Resp Med, Mianyang, Sichuan, Peoples R China

来源：

EUROPEAN RESPIRATORY JOURNAL | 2010年 / 36卷 / 03期

基金：

中国国家自然科学基金;

关键词：

Astragaloside IV; beta-defensin; nuclear factor-kappa B; smoke; OBSTRUCTIVE PULMONARY-DISEASE; ASTRAGALOSIDE-IV; EPITHELIAL-CELLS; HUMAN BETA-DEFENSIN-2; OXIDATIVE STRESS; NITRIC-OXIDE; IN-VITRO; INHIBITION; EXTRACT; INNATE;

D O I：

10.1183/09031936.00029409

中图分类号：

R56 [呼吸系及胸部疾病];

学科分类号：

摘要：

beta-defensin 2 (BD-2), an antimicrobial peptide, participates in airway defence. Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease. This study mainly aims to investigate the effect of CS on rat BD-2 (rBD-2) expression in rat airways. Rats were exposed to CS and treated with caffeic acid phenethyl ester (CAPE), a nuclear factor (NF)-kappa B inhibitor, or astragaloside IV (AS-IV), an active ingredient of Astragalus mongholicus. Besides the analysis of bronchoalveolar lavage fluid (BALF) and histological changes after CS exposure, rBD-2 expression was investigated with immunohistochemistry, reverse transcription PCR and ELISA. Total glutathione and nitric oxide (NO) levels in rat lungs were also detected. CS exposure markedly increased rBD-2 immunoreactivity, as well as rBD-2 mRNA and protein levels in rat airways, which were inhibited by CAPE treatment. Moreover, associated airway inflammation induced by CS was demonstrated by histological changes, increased cell counts and pro-inflammatory cytokines in BALF, and NF-kappa B activation and high levels of total glutathione and NO, which were all reversed by AS-IV in a dose-dependent fashion. In conclusion, CS exposure induces rBD-2 expression in rat airways via a NF-kappa B-dependent pathway, and AS-IV attenuates CS-induced airway inflammation due to its anti-inflammatory and antioxidant properties, at least partly through NF-kappa B inactivation.

引用

页码：638 / 645

页数：8

共 39 条

[1] Blockade of advanced glycation end product formation attenuates bleomycin-induced pulmonary fibrosis in rats [J].