烟草科技2017，Vol.50Issue(10)：35-41,7.
巴豆醛诱导人支气管上皮细胞(BEAS-2B)自噬及相关通路的时间效应变化
Time-effect on alterations of autophagy and related pathways in human bronchial epithelial cells BEAS-2B exposed to crotonaldehyde
王利蒙 1李翔 2杨陟华 3朱茂祥 4谢剑平4
作者信息
- 1. 中国科学院大连化学物理研究所,辽宁省大连市中山路457号116023
- 2. 中国科学院大学,北京市石景山区玉泉路19号100049
- 3. 中国烟草总公司郑州烟草研究院,郑州高新技术产业开发区枫杨街2号450001
- 4. 军事医学科学院放射与辐射医学研究所,北京市太平路27号100850
- 折叠
摘要
Abstract
To assess the toxic effects of crotonaldehyde on human bronchial epithelial cells BEAS-2B,cell counting kit-8(CCK-8)assay was adopted to detect the viability of BEAS-2B cells; immunofluorescence assay to the accumulation and location of autophagosomes; and Western Blot assay to autophagy-marker microtubule-associated protein 1 light chain 3 beta(LC3B-II), the variations of two pathways of phosphatidylinositol 3-kinase(PI3K)/ protein kinase B(Akt)/ mammalian target of rapamycin(mTOR)and liver kinase B1(LKB1)/adenosine monophosphate-activated protein kinase(AMPK)/ Unc-51-like kinase 1 (ULK1). The results indicated that:1)The viability of BEAS-2B cells decreased significantly after exposure to crotonaldehyde. 2)Crotonaldehyde significantly promoted the accumulation of autophagosomes and changed the expression level of LC3B-II. Induced autophagy had apparent time-effect relationship. The level of autophagy in BEAS-2B cells was up-regulated prior to down-regulation with the increase of exposure time. 3)The relative expression of phospho-(P-)PI3K,P-Akt and P-4E-binding protein1(4E-BP1)in PI3K/Akt/mTOR pathway decreased,while that of P-mTOR and P-ribosomal protein S6 kinase(p70 S6K)decreased first and then increased. The activities of LKB1,AMPK,and ULK1 in LKB1/AMPK/ULK1 pathway increased. Collectively, the two pathways mediated the up-regulation of autophagy in BEAS-2B cells exposed to crotonaldehyde.关键词
巴豆醛/人支气管上皮细胞/自噬/PI3K/AMPKKey words
Crotonaldehyde/Human bronchial epithelial cell/Autophagy/PI3K/AMPK分类
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王利蒙,李翔,杨陟华,朱茂祥,谢剑平..巴豆醛诱导人支气管上皮细胞(BEAS-2B)自噬及相关通路的时间效应变化[J].烟草科技,2017,50(10):35-41,7.
