Crotonaldehyde induces apoptosis and immunosuppression in alveolar macrophages

被引:22
|
作者
Yang, Bi-cheng [1 ,2 ]
Yang, Zhi-hua [3 ]
Pan, Xiu-jie [3 ]
Liu, Xing-yu [4 ]
Zhu, Mao-xiang [3 ]
Xie, Jian-ping [2 ]
机构
[1] Chinese Acad Sci, Dalian Inst Chem Phys, Dalian 116023, Liaoning, Peoples R China
[2] Zhengzhou Tobacco Res Inst CNTC, Zhengzhou 450001, Henan, Peoples R China
[3] Beijing Inst Radiat Med, Dept Radiat Toxicol & Oncol, Beijing 100850, Peoples R China
[4] Shanghai Tobacco Corp, Ctr Technol, Beijing Work Stn, Beijing 101121, Peoples R China
关键词
Crotonaldehyde; Apoptosis; Immunosuppression; Alveolar macrophages; BRONCHIAL EPITHELIAL-CELLS; KAPPA-B ACTIVATION; CIGARETTE-SMOKE; OXIDATIVE STRESS; GAS-CHROMATOGRAPHY; GENE-EXPRESSION; TOBACCO-SMOKE; ACROLEIN; PHAGOCYTOSIS; INHIBITION;
D O I
10.1016/j.tiv.2012.09.008
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Crotonaldehyde, a highly toxic alpha, beta-unsaturated aldehyde, is a major component of cigarette smoke (CS) and a ubiquitous environmental pollutant. Exposure to crotonaldehyde-rich pollutants such as CS is associated with suppression of respiratory host defense against infections. The aim of this study was to evaluate the apoptotic and immunological effects of crotonaldehyde exposure in a rat alveolar macrophage (AM) cell line, NR8383. Our studies showed that crotonaldehyde induced AM cell death mainly via the apoptotic process. Crotonaldehyde also decreased the phagocytic activity of AMs. Crotonaldehyde caused inhibition of NO, TNF-alpha, IL-1 beta and IL-12 production in AMs treated with lipopolysaccharide (LPS), which is probably related to inhibition of NF-kappa B activation. These results indicate that crotonaldehyde can cause adverse effects in AMs via multiple mechanisms, and may contribute to compromised lung immunological response in smokers. (C) 2012 Elsevier Ltd. All rights reserved.
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页码:128 / 137
页数:10
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