期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 13, 期 1, 页码 73-81出版社
ELSEVIER
DOI: 10.1016/j.intimp.2012.03.006
关键词
Inflammation; Mucin; Oxidative stress; Quercetin; Smoke
资金
- National Natural Science Foundation of China [30971327, 30900658, 31171103]
- China Medical Board of New York [00-722, 06-834]
- New Doctoral Youth Fund [20090181120109]
Mucus hypersecretion is a feature of many chronic airway diseases induced by cigarette smoke (CS), and evidence suggests that the antioxidant and anti-inflammatory flavonoid quercetin may protect against CS-induced respiratory pathology. In this study, the ability of quercetin to protect against CS-induced mucin expression was examined in vivo and in vitro. Quercetin or 0.2% Tween aqueous solution was administered intraperitoneally to rats, which were then exposed to CS for 28 days. Cell counts and pro-inflammatory cytokine levels were measured in bronchoalveolar lavage fluid (BALF). Lung tissue was examined for total glutathione (GSH) and total antioxidant capacity (T-AOC), histopathological lesions, goblet cell hyperplasia, epidermal growth factor receptor (EGER) phosphorylation and NF-kappa B pathway activation. To complement these in vitro studies, human airway epithelial NCI-H292 cells were pretreated with quercetin and then exposed to cigarette smoke extract (CSE). Cell lysates were examined for Muc5ac expression, EGFR phosphorylation and NF-kappa B pathway activation. In vivo, quercetin pretreatment suppressed CS-induced goblet cell hyperplasia, inflammation, oxidative stress, EGFR phosphorylation and NF-kappa B pathway activation in rat lung. In vitro, quercetin pretreatment attenuated the CSE-induced Muc5ac expression, NF-kappa B activation and EGFR phosphorylation. Our results suggest that quercetin attenuates CS-induced mucin protein synthesis in rat lung, possibly by inhibiting oxidative stress and inflammation via a mechanism involving NF-kappa B pathway activation and EGFR phosphorylation. These findings suggest that quercetin has a potential for treating chronic airway diseases. (C) 2012 Elsevier B.V. All rights reserved.
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