RT Journal Article SR Electronic T1 Cigarette smoke enhances β-defensin 2 expression in rat airways via nuclear factor-κB activation JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP 638 OP 645 DO 10.1183/09031936.00029409 VO 36 IS 3 A1 L. Chen A1 B-B. Sun A1 T. Wang A1 X. Wang A1 J-Q. Li A1 H-X. Wang A1 S-F. Zhang A1 D-S. Liu A1 L. Liu A1 D. Xu A1 X-M. Ou A1 Y-J. Chen A1 T. Yang A1 H. Zhou A1 F-Q. Wen YR 2010 UL http://erj.ersjournals.com/content/36/3/638.abstract AB β-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)-κB 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-κB 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-κB-dependent pathway, and AS-IV attenuates CS-induced airway inflammation due to its anti-inflammatory and antioxidant properties, at least partly through NF-κB inactivation.