期刊文献+

二氧化硒诱导肺腺癌SPCA-1细胞凋亡的研究 被引量:3

Induction of apoptosis in human lung carcinoma SPCA-1 cell line by selenium dioxide(SeO_2)
下载PDF
导出
摘要 目的 :研究二氧化硒诱导肺腺癌细胞系SPCA - 1细胞凋亡。方法 :采用台盼兰拒染法和四甲基偶氮唑蓝 (MTT)比色法测定不同浓度二氧化硒作用不同时间对肺癌SPCA - 1细胞生长的抑制作用 ;采用流式细胞 (FCM)技术 ,观察二氧化硒作用后SP CA - 1细胞的凋亡率及细胞周期的变化 ;通过HE染色和透射电镜观察SPCA - 1细胞的形态变化。结果 :二氧化硒可有效的地抑制SPCA - 1细胞的生长 ,具有时间、浓度依赖性 ;二氧化硒诱导SPCA - 1细胞的凋亡具有浓度依赖性 ;二氧化硒低浓度时阻滞SPCA - 1细胞于S期 ,高浓度时选择性诱导S期细胞凋亡 ;二氧化硒作用后 ,SPCA - 1细胞呈现典型的凋亡细胞形态特征。结论 :二氧化硒通过诱导S期细胞凋亡而抑制肺腺癌细胞系SPCA - 1细胞的生长 ,具有时效。 Objective To study apoptosis of lung carcinoma SPCA-1 cell line induced by SeO 2. Methods: Trypan blue dying and Methyl thiazolyl tetrazolium(MTT) was used to observe the growth inhibition rates of SPCA-1 cells by various concentration of SeO 2 at different time ponts. Apoptosis percentage and cell cycle phase distribution of SPCA-1 were measured by flow cytometry (FCM) assays. Apoptotic phenotype of SPCA-1 was observed by HE dying and electric microscope . Results: SeO 2 could inhibit the growth of SPCA-1 cells effectively and depended on the action time and concentration of the medicine. SPCA-1 cell apoptotic percentage induced by SeO 2 was enhanced in concentration-dependent pattern. S phase cell of SPCA-1 were arrested in lower concentration of SeO 2, while higher concentration induced apoptosis selectively. SPCA-1 cells treated by SeO 2 showed morphological characteristic of apoptotic cells. Conclusion: SeO 2 can inhibit the proliferation of lung carcinoma SPCA-1 cells by inducing S phase cells apoptosis, and it is time-dependent and concentration-dependent and cell cycle specific.
出处 《西北国防医学杂志》 CAS 2003年第4期253-255,共3页 Medical Journal of National Defending Forces in Northwest China
基金 全军青年基金资助项目 ( 98Q0 10 )
关键词 肺癌 二氧化硒 SPCA—1 凋亡 Lung carcinoma Selenium dioxide SPCA-1 Apoptosis
  • 相关文献

参考文献8

  • 1曹晓哲,邢传平,高自芳,刘华福,董亮.急性硒中毒后小鼠肝细胞线粒体损伤的体视学研究[J].西北国防医学杂志,1999,20(3):169-171. 被引量:6
  • 2Wei Y, Cao X, Ou Y, et al. SeO2 induces apoptosis with down- regulation of Bcl- 2 and up- regulation of p53 expression in both immortal human hepatic cell line and hepatoma cell line[J]. Mutat Res, 2001, 490(2) : 113 - 121.
  • 3Ganther HE. Selenium metabolism, selenoproteins and mechanisms of cancer prevention: complexities with thioredoxin reductase[J]. Carcinogenesis, 1999,20:1657 -1666.
  • 4Sinks R, Medina D. Inhibition of cdk2 kinase activity by methylselenocysteine in synchronized mouse mammary epitlelial tumor cells[J]. Carcinogenesis, 1997,18:1541 - 1547.
  • 5Menter DG, Sabichi AL, Lippman SM. Selenium effects on prostate cell growth [ J ]. Cancer Epidemiol Biomarkers Prev,2000,9(11):1171- 1182.
  • 6Liu S, Shia D, Liu G, et al. Roles of Se and No in apoptosis of hepatoma cells[J]. Life Sic,2000,29:68(6):603- 610.
  • 7Stewart MS, Spallholz JE, Neldner KH, et al. Selenium compounds have disparate abilities to impose oxidative stress and induced apoptosis[J]. Free Radical Biol Med, 1999 ,26:42-48.
  • 8Lu JX, Kaeck M, Jiang C, et al. Selenite induction of DNA strand breaks and apoptosis in mouse leukemic L1210 cells[J].Biochem Pharmacol, 1994,47:531- 535.

二级参考文献7

共引文献5

同被引文献33

引证文献3

二级引证文献10

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