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交通相关细颗粒物对CEM-6T细胞凋亡不同信号通路的影响 被引量:3

Effect of Traffic-related Fine Particulate Matter on Different Signaling Pathways of CEM-6T Cell Apoptosis
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摘要 目的探讨交通相关细颗粒物对CEM-6T细胞凋亡的影响,为研究交通相关细颗粒物的免疫毒性机制提供实验依据。方法使用不同剂量(0、20、80、320μg/ml)交通相关细颗粒物染毒CEM-6T细胞24和48 h,用RT-PCR测定CEM-6T细胞中Caspase-3的mRNA表达,以Western Blot测定Caspase-9、Cyt-c、Fas-L、Caspase-8和TNF-α蛋白表达。结果 320μg/ml交通相关细颗粒物染毒细胞24 h和48 h后,Caspase-3基因表达高于对照组,差异有统计学意义(P<0.05)。80、320μg/ml细颗粒物染毒细胞24和48 h后,细胞内Cyt-C、Caspase-9、Fas-L、Caspase-8、TNF-α蛋白表达升高,与对照组比较,差异有统计学意义(P<0.05)。结论交通相关细颗粒物可通过线粒体通道和死亡受体通道诱导CEM-6T细胞凋亡。 Objective To investigate the effect of traffic-related fine particulate matter on CEM-6T cell apoptosis and provide experimental basis for the immunotoxieity mechanism. Methods CEM-6T cells were exposed to different doses of traffic-related fine particulate matter (0, 20, 80 and 320 μg/ml) for 24 h and 48 h respectively. The mRNA expression of Caspase-3 was determined by RT-PCR. The protein expression of Caspase-9, Cyt-c, Fas-L, Caspase-8 and TNF-α were detected by Western Blot. Results CEM-6T cells were exposed to 320 μg/ml of traffic-related fine particulate matter for 24 h and 48 h, the Caspase-3 mRNA expression increased significantly compared with saline control group (P〈0.05). When the cells were exposed to 80 and 320 μg/ml of fine particulate for 24 h and 48 h, the protein expression of Cyt-c, Caspase-9, Fas-L, Caspase-8 and TNF-α enhanced, the differences with the saline control group were statistically significant(P〈0.05). Conclusion Traffic-related fine particulate matter may induce CEM-6T apoptosis through the mitochondrial and death receptor pathway.
出处 《环境与健康杂志》 CAS CSCD 北大核心 2011年第12期1062-1064,共3页 Journal of Environment and Health
基金 国家自然科学基金(30700655) 2009年度山西省高等学校优秀青年学术带头人支持项目
关键词 PM2.5 汽车尾气 CEM-6T 凋亡 PM2.5 Automobile exhaust CEM-6T Apoptosis
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  • 1彭瑞玲,刘君卓,潘小川,刘红,温天佑,金晓滨,陈波.3种民用燃料的燃烧颗粒物的含量及其粒径组成[J].环境与健康杂志,2005,22(1):13-15. 被引量:9
  • 2张浩,梁英,曾祥贵,刘勇,林川,蔡春华,吴德生.以甲醇和汽油为燃料的汽车尾气对RAW264.7细胞的细胞毒性及对其增殖和凋亡的影响[J].环境与健康杂志,2005,22(5):332-335. 被引量:2
  • 3Hertz-Picciotto I, Herr CE, Yap PS, et al. Air pollution and lymphocyte phenotype proportions in cord blood [J]. Environ Health Perspect,2005, 113:1391-1398.
  • 4Mamman A, Simpson JP, Nighorn A, et al.Hippocalcin in the olfactory epithelium:a mediator of second messenger signaling [J].Biochem Biophys Res Commun, 2004, 322 : 1131-1139.
  • 5Helmreich EJ.Environmental influences on singal transduction throuhg membranes : a retrospective mini-review [ J ].Biophys Chem, 2003,100: 519-534.
  • 6Cakmak S, Dales RE, Vida CB. Components of particulate air pollution and mortality in Chile [J]. Int J Occup Environ Health, 2009,15:152- 158.
  • 7Parker JD, Akinbami LJ, Woodruff TJ. Air pollution and childhood respiratory allergies in the United States [J]. Environ Health Perspect, 2009,117:140-147.
  • 8Zhao XH, Wang XL, Li XY. Automobile exhaust particle-induced apoptosis and necrosis in MRC-5 cells [J]. Toxicol Lett,2001, 122: 103-110.
  • 9Burchiel SW, Luster MI.Signaling by environmental polycyclic aromatic hydrocarbons in human lymphoeytes [J].Clindamyein Hydrochloride Clin Immunol, 2001, 98:2-10.
  • 10Schwartz J, Laden F, Zanobetti A. The concentration-response relation between PM2.5 and daily deaths[J]. Environ Health Perspect,2002,110(10):1025.

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