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题名: Crotonaldehyde induces autophagy-mediated cytotoxicity in human bronchial epithelial cells via PI3K, AMPK and MAPK pathways
作者: Wang, Limeng1, 2;  Li, Xiang3;  Yang, Zhihua4;  Pan, Xiujie4;  Liu, Xingyu5;  Zhu, Maoxiang4;  Xie, Jianping3
关键词: Crotonaldehyde ;  Autophagy ;  PI3K ;  AMPK ;  MAPK
刊名: ENVIRONMENTAL POLLUTION
发表日期: 2017-09-01
DOI: 10.1016/j.envpol.2017.03.083
卷: 228, 页:287-296
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology ;  Life Sciences & Biomedicine
类目[WOS]: Environmental Sciences
研究领域[WOS]: Environmental Sciences & Ecology
英文摘要: Crotonaldehyde is an ubiquitous hazardous pollutant in the environment which can be produced naturally, artificially and endogenously. Acute exposure of crotonaldehyde was reported to induce severe lung injury in humans and experimental animals. However, the exact toxicity mechanisms of crotonaldehyde in organisms have not been fully explored. In the present study, we explored the role autophagy played in the cytotoxicity induced by crotonaldehyde in human bronchial epithelial cells (BEAS-2B), and the pathways that mediated autophagy, including the phosphatidylinositol 3-kinase (PI3K) pathway, the AMP-activated protein kinase (AMPK) pathway and the mitogen-activated protein kinase (MAPK) pathways, were examined and validated. We found that crotonaldehyde induced cytotoxicity and autophagy simultaneously in BEAS-2B cells, and blockage of autophagic flux significantly elevated the viability of BEAS-2B exposed to high concentrations of crotonaldehyde. Crotonaldehyde down regulated the activity of PI3K pathway, and elevated the activities of AMPK and MAPK pathways. Pretreatment of specific agonist or antagonist of these pathways could inhibit autophagy and partly improve the viability. These results suggested that acute exposure of crotonaldehyde induced cell death mediated by autophagy, which might be helpful to elucidate the toxicity mechanisms of crotonaldehyde and contribute to environmental and human health risk assessment. (C) 2017 Elsevier Ltd. All rights reserved.
关键词[WOS]: APOPTOSIS ;  INHIBITION ;  EXPRESSION ;  DISEASE ;  DEATH ;  RATS ;  PHOSPHORYLATION ;  1,3-BUTADIENE ;  PATHOGENESIS ;  MACROPHAGES
语种: 英语
WOS记录号: WOS:000405042100030
Citation statistics: 
内容类型: 期刊论文
URI标识: http://cas-ir.dicp.ac.cn/handle/321008/152066
Appears in Collections:中国科学院大连化学物理研究所_期刊论文

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作者单位: 1.Chinese Acad Sci, Dalian Inst Chem Phys, Key Lab Separat Sci Analyt Chem, 457 Zhongshan Rd, Dalian 116023, Peoples R China
2.Univ Chinese Acad Sci, 19 Yuquan Rd, Beijing 100049, Peoples R China
3.Zhengzhou Tobacco Res Inst CNTC, Key Lab Tobacco Chem, 2 Fengyang Rd, Zhengzhou 450001, Peoples R China
4.Beijing Inst Radiat Med, Dept Radiat Toxicol & Oncol, 27 Taiping Rd, Beijing 100850, Peoples R China
5.Shanghai Tobacco Grp Corp CNTC, 99 Wansheng South St, Beijing 101121, Peoples R China

Recommended Citation:
Wang, Limeng,Li, Xiang,Yang, Zhihua,et al. Crotonaldehyde induces autophagy-mediated cytotoxicity in human bronchial epithelial cells via PI3K, AMPK and MAPK pathways[J]. ENVIRONMENTAL POLLUTION,2017,228:287-296.
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