title: Quercetin attenuates airway inflammation and mucus production induced by cigarette smoke in rats.
abstract: 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 (EGFR) phosphorylation and NF-κB 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-κB pathway activation. In vivo, quercetin pretreatment suppressed CS-induced goblet cell hyperplasia, inflammation, oxidative stress, EGFR phosphorylation and NF-κB pathway activation in rat lung. In vitro, quercetin pretreatment attenuated the CSE-induced Muc5ac expression, NF-κB 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-κB pathway activation and EGFR phosphorylation. These findings suggest that quercetin has a potential for treating chronic airway diseases.
authors.affiliation: Division of Pulmonary Disease, State Key Laboratory of Biotherapy and Department of Respiratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, PR China.
authors.forename: Ting
authors.initials: T
authors.lastname: Yang
authors.forename: Feng
authors.initials: F
authors.lastname: Luo
authors.forename: Yongchun
authors.initials: Y
authors.lastname: Shen
authors.forename: Jing
authors.initials: J
authors.lastname: An
authors.forename: Xiaoou
authors.initials: X
authors.lastname: Li
authors.forename: Xinyu
authors.initials: X
authors.lastname: Liu
authors.forename: Binwu
authors.initials: B
authors.lastname: Ying
authors.forename: Zenglin
authors.initials: Z
authors.lastname: Liao
authors.forename: Jiajia
authors.initials: J
authors.lastname: Dong
authors.forename: Lingli
authors.initials: L
authors.lastname: Guo
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Dan
authors.initials: D
authors.lastname: Xu
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: Fuqiang
authors.initials: F
authors.lastname: Wen
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use*; D015153:Blotting, Western; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000276:immunology; D002452:Cell Count; D002460:Cell Line; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D006801:Humans; D008297:Male; D055271:Mucin 5AC / Q000096:biosynthesis; D018384:Oxidative Stress; D011014:Pneumonia / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D011794:Quercetin / Q000008:administration & dosage / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020545:Respiratory Mucosa / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012906:Smoke / Q000009:adverse effects*; D014026:Nicotiana
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C524678:MUC5AC protein, human; D055271:Mucin 5AC; D012906:Smoke; D011794:Quercetin