期刊文献+

放射性核素^(89)Sr诱发K_(562)癌细胞凋亡的放射毒理效应的分子机理研究 被引量:1

THE CHARACTERISTICS AND MECHANISM OF APOPTOSIS IN K_(562) CELLS INDUCED BY RADIONUCLIDES STRONTIUM-89
下载PDF
导出
摘要 采用分子病理和定量病理技术研究放射性核素89Sr诱导的K562癌细胞凋亡、剂量效应关系和重要相关基因bcl-2和bax在其中的表达。结果表明,K562细胞经89Sr作用达6h和24h,提取DNA,琼脂糖凝胶电泳图谱上出现典型的“阶梯状”区带,伴有“拖尾”,面对照组未见“阶梯状”区带:荧光双标记流式细胞仪法定量检测见89Sr作用6、9、12、24和48h后,K562细胞凋亡率、K562细胞坏死率均较对照组有明显的升高(p<0.01)。免疫组织化学染色显示,对照组K562细胞中bcl-2、bax均何表达,bcl-2表达阳性细胞率82.8%,bax表达阳性细胞率44.4%,bcl-2/bax比值1.86,89Sr作用24h后的K562细胞中,bcl-2表达阳性细胞率31.4%,bax表达阳性细胞率38.2%,bcl-2/bax比值0.82与对照组相比,差异具有显著性(p<0.05);结果显示,放射性核素89Sr照射K562细胞后,细胞凋亡与细胞坏死并存,且89Sr诱导K562细胞的凋亡可能是通过bcl-2表达蛋白降低,bcl-2/bax比值下降而调控的。 In this paper, apoptosis and expressions of bcl-2 and bax protein in K562 cells exposed to different doses of strontium-89 were studied. Six hours after the irradiation, characteristics of apoptosis and necrosis appeared in the K562 cells. The apoptosis and necrosis in the cells irradiated for 6, 9, 12, 24 and 48h were significantly higher than the control. The expression of bcl-2 decreased after the irradiation, whereas bax had no obvious changes. The results suggested that the apoptosis of K562 cells induced by exposure to 89Sr might be regulated by reduced expression of bcl-2 and bcl-2/bax ratio.
出处 《辐射研究与辐射工艺学报》 CAS CSCD 北大核心 2003年第1期77-80,共4页 Journal of Radiation Research and Radiation Processing
基金 苏州大学附属第一临床学院资助课题
关键词 放射性核素 K562癌细胞 放射毒理效应 分子机理 ^89SR K562细胞 肿瘤 细胞凋亡 临床治疗 Strontium-89, K_(562) cells, Apoptosis, Bcl-2, Bax
  • 相关文献

参考文献16

  • 1Kerr J F R, Winterfor C M, Harmon B V et al. Cancer, 1994, 73:2013-2015
  • 2分子克隆实验指南.北京:科学出版社,1992, 304Molecular Cloning Laboratory Manual.Beijing:Science and Techniques Publisher, 1992, 304
  • 3基因工程实验技术.长沙:湖南科学技术出版社,1997, 1Gene Engineering Laboratory Techniques.Changsha:Hunan Science and Techniques Publisher, 1997:1
  • 4Afanasyev V N, Korol B A, Matylevich N P et al. Cytometry,1993, 14:603-608
  • 5Vitale M, Zamai L, Mazzotti G et al. Histochemistry, 1993, 100:223-226
  • 6Huschtscha L, Jeitner T M, Andersoin C E et al. Exp Cell Res, 1994, 212:161-164
  • 7浓缩铀的放射毒理.北京:原子能出版社, 1998, 125Radiotoxicology of Enriched Uranium. Beijing: Atomic Energy Publisher, 1998,125
  • 8Forster T H, Allan D J, Gobe G C et al. Int J Radiat Bilo, 1992, 61(3):365-367
  • 9朱寿彭,肖东,韩晓枫.DNA凝胶电泳和放射自显影研究^(153)Sm诱发骨肉瘤细胞凋亡[J].中华放射医学与防护杂志,1999,19(5):307-309. 被引量:4
  • 10朱寿彭,肖东,韩晓枫.^(153)Sm-EDTMP诱发骨肉瘤细胞凋亡的荧光显微镜形态和增生抑制研究[J].核技术,1999,22(5):309-311. 被引量:3

二级参考文献25

共引文献14

同被引文献11

  • 1Kerr J F, Wyllie A H, Currie A R. Apoptosis: A Basic Biological Phenomenon with Wide-ranging lmplications in Tissue kinetics. Br. J. Cancer, 1972. 26:239.
  • 2Prindull G. Apoptosis in the Embryo and Tumorigenesis. Eur. J. Cancer, 1995. 31a:116.
  • 3Thompson C B. Apoptosis in the Pathogenesis and Treatment of Disease. Science, 1995. 267:1456.
  • 4Akagi Y, Ito K, Sawada S. Radiation-induced Apoptosis and Necrosis in Molt-4 Cells: A Study of Dose-effect Relationships and Their Modification. Int. J. Radiat. Biol., 1993. 64(1) : 47.
  • 5Chou R H, Huang H. Restoration of p53 Tumor Suppressor Pathway in Human Cervical Carcinoma Cells by Sodium Arsenite. Biochem. Biophys. Res. Commun., 2002. 293(1):298.
  • 6Schimmer A D, Hedley D W, Penn L Z, et al. Receptor-and Mitochondrial-mediated Apoptosis in Acute Leukemia: A Translational View. Blood, 2001. 98(13) : 3542.
  • 7Danial N N, Korsmeyer S J. Cell Death: Critical Control Points. Cell,2004. 16:205.
  • 8赵卫红,陈家佩,从玉文,郑胡镛.γ射线诱导HL-60和K562细胞凋亡和G_2期阻滞的关系[J].基础医学与临床,2000,20(2):71-73. 被引量:7
  • 9薛丽香,金光辉,付士波,苏旭.电离辐射对EL-4细胞凋亡与坏死的影响[J].中华放射医学与防护杂志,2001,21(1):24-26. 被引量:4
  • 10许建华,杨占山,杨淑琴,王春雷,姜建平.^(60)Coγ射线诱导的K562细胞增殖抑制和凋亡的研究[J].苏州大学学报(医学版),2002,22(6):665-667. 被引量:1

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部