Apple polyphenol protects against cigarette smoke-induced acute lung injury

被引:61
作者
Bao, Meng-Jing [1 ]
Shen, Jian [1 ]
Jia, Yong-Liang [2 ]
Li, Fen-Fen [1 ]
Ma, Wen-Jiang [1 ]
Shen, Hui-Juan [1 ]
Shen, Liang-Liang [1 ]
Lin, Xi-Xi [1 ]
Zhang, Lin-Hui [1 ]
Dong, Xin-Wei [1 ]
Xie, Yi-Cheng [1 ]
Zhao, Yu-Qing [2 ]
Xie, Qiang-Min [1 ]
机构
[1] Zhejiang Univ, Zhejiang Resp Drugs Res Lab State Food & Drug Adm, Coll Med, Hangzhou 310058, Zhejiang, Peoples R China
[2] Shenyang Pharmaceut Univ, Dept Tradit Chinese Mat Med, Shenyang 110016, Peoples R China
基金
中国国家自然科学基金;
关键词
Apple polyphenol; Cigarette smoke; Free radicals; Oxidative stress; Lung inflammation; OBSTRUCTIVE PULMONARY-DISEASE; EPITHELIAL-CELLS; OXIDATIVE STRESS; GENE-EXPRESSION; IN-VITRO; T-CELLS; COPD; EXTRACT; ASTHMA; INFLAMMATION;
D O I
10.1016/j.nut.2012.04.008
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 [营养与食品卫生学];
摘要
Objective: Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease involving oxidative stress as well as a wide variety of cells activated from smoking cigarettes. There have been disappointingly few therapeutic advances in drug therapy for COPD. Plant polyphenols have been the topic of much research regarding their antioxidant activities and antiinflammatory and immunomodulatory effects. In the present study, we ask whether apple polyphenol provides protection against cigarette smoke (CS)-induced acute lung injury. Methods: ICR mice were exposed to CS for 4 d with increasing exposure time for up to 6 h per day to elicit epithelial cells injury. One hour before smoke exposure, mice were treated with apple polyphenol (APP) by gavage; all examinations were performed 18 h after the last CS exposure. Results: APP at 30, 100, or 300 mg not only significantly dose-dependently reduced the CS-induced accumulation of inflammatory cells and gene/protein expression of proinflammatory factors both in the lung and in bronchoalveolar lavage fluid, but also significantly reversed oxidative stress in the lungs. Additionally, treatment with APP also significantly regulated the CS-induced imbalance of matrix metalloproteinases-9/tissue inhibitor of metalloproteinase-1 expression in the lungs. To investigate further the possible signaling pathway of APP effects, we examined protein expression of p-P38 MAPK by immunohistochemistry that found treatment with APP significantly decreased the CS-induced increases of p-P38 expression in the lungs. Conclusion: Taken together, APP may be a potential dietary nutrient supplement agent to improve quality of life of COPD patients by inhibiting CS-exposed acute lung injury via P38 MAPK signaling pathway. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:235 / 243
页数:9
相关论文
共 42 条
[1]
Characteristics and physiological functions of polyphenols from apples [J].
Akazome, Y .
BIOFACTORS, 2004, 22 (1-4) :311-314
[3]
Barnes PJ, 2000, AM J RESP CRIT CARE, V161, P342
[4]
The p38/RK mitogen-activated protein kinase pathway regulates interleukin-6 synthesis in response to tumour necrosis factor [J].
Beyaert, R ;
Cuenda, A ;
VandenBerghe, W ;
Plaisance, S ;
Lee, JC ;
Haegeman, G ;
Cohen, P ;
Fiers, W .
EMBO JOURNAL, 1996, 15 (08) :1914-1923
[5]
Exhaled breath condensate biomarkers in COPD [J].
Borrill, Z. L. ;
Roy, K. ;
Singh, D. .
EUROPEAN RESPIRATORY JOURNAL, 2008, 32 (02) :472-486
[6]
NRF2 targeting: a promising therapeutic strategy in chronic obstructive pulmonary disease [J].
Boutten, A. ;
Goven, D. ;
Artaud-Macari, E. ;
Boczkowski, J. ;
Bonay, M. .
TRENDS IN MOLECULAR MEDICINE, 2011, 17 (07) :363-371
[7]
Polyphenols: Planting the seeds of treatment for the metabolic syndrome [J].
Cherniack, E. Paul .
NUTRITION, 2011, 27 (06) :617-623
[8]
Cytokines as targets in chronic obstructive pulmonary disease [J].
Chung, K. F. .
CURRENT DRUG TARGETS, 2006, 7 (06) :675-681
[9]
Effect of an MMP-9/MMP-12 inhibitor on smoke-induced emphysema and airway remodelling in guinea pigs [J].
Churg, Andrew ;
Wang, Rona ;
Wang, Xiaoshan ;
Onnervik, Per-Ola ;
Thim, Kerstin ;
Wright, Joanne L. .
THORAX, 2007, 62 (08) :706-713
[10]
Late Intervention with a Myeloperoxidase Inhibitor Stops Progression of Experimental Chronic Obstructive Pulmonary Disease [J].
Churg, Andrew ;
Marshall, Caroline V. ;
Sin, Don D. ;
Bolton, Sarah ;
Zhou, Steven ;
Thain, Katherine ;
Cadogan, Elaine B. ;
Maltby, Justine ;
Soars, Matthew G. ;
Mallinder, Philip R. ;
Wright, Joanne L. .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2012, 185 (01) :34-43