[1]杨 萨),周洋洋),张佳彤),等.烟草烟雾凝集物对BEAS-2B细胞氧化应激的影响[J].郑州大学学报(医学版),2019,(04):517-521.[doi:10.13705/j.issn.1671-6825.2018.10.058]
 YANG Sa),ZHOU Yangyang),ZHANG Jiatong),et al.Effects of cigarette smoke condensate on oxidative stress in BEAS-2B cells[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2019,(04):517-521.[doi:10.13705/j.issn.1671-6825.2018.10.058]
点击复制

烟草烟雾凝集物对BEAS-2B细胞氧化应激的影响()
分享到:

《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2019年04期
页码:
517-521
栏目:
论著
出版日期:
2019-07-20

文章信息/Info

Title:
Effects of cigarette smoke condensate on oxidative stress in BEAS-2B cells
作者:
杨 萨1)周洋洋1)张佳彤2)李中秋1)于 琪1)栗振凯1)殷晓涵1)张 巧1)
1)郑州大学公共卫生学院卫生毒理学教研室 郑州 450001;2)郑州大学医院疾病预防控制科 郑州 450001
Author(s):
YANG Sa1)ZHOU Yangyang1)ZHANG Jiatong2)LI Zhongqiu1)YU Qi1)LI Zhenkai1)YIN Xiaohan1)ZHANG Qiao1)
1)Department of Toxicology, College of Public Health, Zhengzhou University, Zhengzhou 450001;2)Department of Disease Prevention and Control, Zhengzhou University Hospital, Zhengzhou 450001
关键词:
烟草烟雾凝集物 BEAS-2B细胞 氧化应激
Keywords:
cigarette smoke condensate BEAS-2B cell oxidative stress
分类号:
R114
DOI:
10.13705/j.issn.1671-6825.2018.10.058
摘要:
目的:研究烟草烟雾凝集物(CSC)对BEAS-2B细胞氧化应激的影响。方法:采用0.02、0.04、0.06和0.08 g/L的CSC染毒BEAS-2B细胞24 h,并设立空白对照组和DMSO溶剂对照组。分别用CCK-8法和划痕实验检测细胞存活率和细胞迁移能力,荧光探针DCFH-DA法检测BEAS-2B细胞内活性氧(ROS)水平,酶标仪测定细胞内丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性。结果:CCK-8结果显示CSC以剂量依赖性的方式降低BEAS-2B细胞存活率; 随着CSC浓度的升高,细胞出现空泡增多、针刺样突起、细胞膜及细胞核轮廓模糊、细胞面积明显增大等形态学改变。与空白对照组、DMSO溶剂对照组相比,CSC染毒组细胞迁移距离增加,细胞内ROS水平、MDA含量升高,SOD活性降低(P<0.05)。结论:CSC可引起BEAS-2B细胞发生氧化应激反应。
Abstract:
Aim:To investigate the effects of cigarette smoke condensate(CSC)on oxidative stress in BEAS-2B cells.Methods:BEAS-2B cells were exposed to CSC at concentrations of 0.02, 0.04, 0.06, and 0.08 g/L for 24 hours, and a blank control group and a DMSO solvent control group were established. Cell toxicity of CSC to BEAS-2B cells were tested by CCK-8 assay. Scratch test was used to detect cell migration ability. The changes of intracellular reactive oxygen species(ROS), malondialdehyde(MDA)and superoxide dismutase(SOD)were measured by fluorescent probe DCFH-DA and microplate reader.Results:CSC decreased cell viability in a dose-dependent manner, and changed the characteristics of cell morphology. Compared with the blank control group and the DMSO solvent control group, the migration distance and the levels of ROS and MDA increased, and SOD activity decreased in CSC groups(P<0.05).Conclusion:CSC could induce the occurrence of oxidative stress in BEAS-2B cells.

参考文献/References:

[1] 马铮,平芬,曹磊,等.香烟烟雾成分对呼吸系统的影响[J].国际呼吸杂志,2015,35(4):313
[2] WORLD HEALTH ORGANIZATION.The world health report 2002[J].Midwifery,2003,19(1):72
[3] 李广康,陈健东,孙东杰,等.烟草烟雾凝集物对BEAS-2B细胞caspase-1及相关炎性细胞因子表达的影响[J].毒理学杂志,2015,29(6):440
[4] CUADRADO A,NEBREDA AR.Mechanisms and functions of p38 MAPK signalling[J].Biochem J,2010,429(3):403
[5] SCULIER JP,BERGHMANS T,MEERT AP.Update in lung cancer and mesothelioma 2009[J].Am J Respir Crit Care Med,2010,181(8):773
[6] SMITH CJ,PERFETTI TA,GARG R,et al.IARC carcinogens reported in cigarette mainstream smoke and their calculated log P values[J].Food Chem Toxicol,2003,41(6):807
[7] 胡成平.肺癌流行病学与烟草控制的研究进展[J].中国肺癌杂志,2008,11(1):25
[8] 李洋.醛固酮经非基因组途径激活氧化应激通路调控大鼠肝星状细胞收缩迁移的机制研究[D].广州:南方医科大学,2014.
[9] 黄畅宇,戴爱国.香烟烟雾对细胞生物学功能的影响[J].国际呼吸杂志,2012,32(16):1278
[10]POPE CA,BURNETT RT,TURNER MC,et al.Lung cancer and cardiovascular disease mortality associated with ambient air pollution and cigarette smoke: shape of the exposure-response relationships[J].Environ Health Perspect,2011,119(11):1616
[11]RENNARD SI.Cigarette smoke in research[J].Am J Respir Cell Mol Biol,2004,31(5):479
[12]KAMIIDE Y,FURUYA M,INOMATA N,et al.Chronic exposure to cigarette smoke causes extrapulmonary abnormalities in rats[J].Environ Toxicol Pharmacol,2015,39(2):864
[13]ZHANG S,LI X,XIE F,et al.Evaluation of whole cigarette smoke induced oxidative stress in A549 and BEAS-2B cells[J].Environ Toxicol Pharmacol,2017,54:40
[14]CARNEVALI S,PETRUZZELLI S,LONGONI B,et al.Cigarette smoke extract induces oxidative stress and apoptosis in human lung fibroblasts[J].Am J Physiol Lung Cell Mol Physiol,2003,284(6):L955
[15]BAGLOLE CJ,BUSHINSKY SM,GARCIA TM,et al.Differential induction of apoptosis by cigarette smoke extract in primary human lung fibroblast strains: implications for emphysema[J].Am J Physiol Lung Cell Mol Physiol,2006,291(1):L19
[16]SOBINOFF AP,BECKETT EL,JARNICKI AG,et al.Scrambled and fried: cigarette smoke exposure causes antral follicle destruction and oocyte dysfunction through oxidative stress[J].Toxicol Appl Pharmacol,2013,271(2):156
[17]VAN DER TOORN M,REZAYAT D,KAUFFMAN HF,et al.Lipid-soluble components in cigarette smoke induce mitochondrial production of reactive oxygen species in lung epithelial cells[J].Am J Physiol Lung Cell Mol Physiol,2009,297(1):L109

相似文献/References:

[1]曹会敏,倪 静,玉崧成,等.RNAi沉默Nrf2基因增强煤焦沥青烟提取物对BEAS-2B细胞的毒性作用[J].郑州大学学报(医学版),2018,(01):25.[doi:10.13705/j.issn.1671-6825.2017.05.047]
 CAO Huimin,NI Jing,YU Songcheng,et al.The role of RNAi-mediated Nrf2 gene silencing on malignant transformation of BEAS-2B cells induced by coal tar pitch smoke extract[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2018,(04):25.[doi:10.13705/j.issn.1671-6825.2017.05.047]

备注/Memo

备注/Memo:
【基金项目】国家自然科学基金资助项目(81172717)
【作者简介】张巧,通信作者,女,1965年6月生,博士,教授,研究方向:分子与遗传毒理学,E-mail:zhangqiao@zzu.edu.cn
更新日期/Last Update: 2019-07-20