期刊文献+

三氧化二砷对慢性粒细胞白血病细胞系的作用(英文) 被引量:3

Effect of Arsenic Trioxide on Different Cell Lines Derived from Chronic Myeloid Leukemia
暂未订购
导出
摘要 本研究探讨三氧化二砷 (As2 O3)对两种慢性粒细胞白血病 (CML)细胞系有无作用及作用机制。实验选用了两种不同的CML细胞系KU81 2和MEG 0 1及两种其它白血病细胞系U937和PL2 1 ,加入不同浓度的As2 O3(0 .2 ,2和 1 0 μmol/L) ,在不同时间计数活细胞数 ,观察细胞形态 ,并以TUNEL法和DNA凝胶电泳检测细胞有无凋亡的发生 ;同时检测 0 .2 μmol/LAs2 O3作用时细胞表面CD34 ,CD1 3 ,CD33 ,CD1 9,CD1 1b ,CD1 4和CD7的变化 ,并通过RT PCR检测细胞bcr abl水平及caspase 3的变化。研究结果发现 ,不同浓度的As2 O3对 4种细胞系的作用不同 ,1 0 μmol/L时 4种细胞系均会发生细胞凋亡 ,2 μmol/L时则仅CML细胞系KU81 2和MEG 0 1会产生凋亡 ,0 .2μmol/L时 4种细胞系均不发生凋亡。在培养 2 4小时后 ,4种细胞系表面的CD34 ,CD1 3 ,CD33 ,CD1 9,CD1 1b ,CD1 4和CD7等均无明显改变。RT PCR检测bcr abl的水平发现在 2种CML细胞系中无明显改变 ,其caspase 3的活性较对照细胞均有所增加。结论 :As2 O3在较高浓度下可诱导 4种白血病细胞系产生凋亡 ,在 2 μmol/L仅可诱导CML来源的两种细胞系产生凋亡 ,CML细胞系对As2 O3较其它两种细胞系敏感 ,其作用机制与caspase The objective is to explore the effect and the mechanism of arsenic trioxide(As 2O 3) on different cell lines of chronic myeloid leukemia(CML). Different concentrations of As 2O 3 (0.2, 2 and 10 μmol/L) were added to CML cell lines KU812 and MEG 01 and other leukemia cell lines U937 and PL21, the cell numbers were counted at different times, TUNEL and DNA ladder were assayed. Different antibodies, CD34, CD13, CD33, CD19, CD11b, CD14 and CD7, were added to detect the change of the molecules on cell surface, the change of bcr abl by RT PCR and the activity of caspase 3 were assayed. The results showed that different concentrations of As 2O 3 had different effects on the survival of the 4 cell lines. After culture for 24 hours with As 2O 3, there was no significant increase in CD11b in all the four cell lines. There were no changes of bcr abl in the 2 CML cell lines treated and untreated with As 2O 3 by RT PCR. Activities of caspase 3 were all increased. It is concluded that As 2O 3 can induce apoptosis in CML cell lines, the concentration to induce apoptosis is different, CML cell lines are more sensitive than the other 2 leukemia cell lines. As 2O 3 induced apoptosis may have some relation with the activation of caspase 3.
出处 《中国实验血液学杂志》 CAS CSCD 2002年第5期413-418,共6页 Journal of Experimental Hematology
关键词 三氧化二砷 慢性粒细胞白血病细胞系 细胞凋亡 bcr—abl MRNA caspase—3 作用机制 arsenic trioxide chronic myeloid leukemia cell line apoptosis bcr abl mRNA caspase 3
  • 相关文献

参考文献20

  • 1Nitta M, Kato Y, Strife A, et al.Incidence of involvement of the B and T lymphocyte lineages in chronic myelogenousleukemia. Blood,1985; 66:1053 - 1061
  • 2Rowley JD. Letter: a new consistent chromosomal abnormality in chronic myelogenousleukemia identified by quinacrine fluorescence and Giemsa staining. Nature, 1973; 243: 290- 293
  • 3Nowell PC, Hungerford DA. A minute chromosome in human chronic granulocyticleukemia. Science, 1960; 132:1497
  • 4Chen GQ, Zhu J, Shi XG, et al. In vitro studies on cellular and molecularmechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia:As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation ofPMLRAR alpha/PML proteins. Blood, 1996; 88:1052- 1061
  • 5Radich JP, Gehly G, Gooley T, et al. Polymerase chain reaction detection of theBCR-ABL fusion transcript after allogeneic marrow transplantation for chronic myeloidleukemia: results and implications in 346 patients. Blood, 1995; 85:2632 - 2638
  • 6Martin SJ, Lennon SV, Bonham AM, et al. Induction of apoptosis (programmed celldeath ) in human leukemic HL-60 cells by inhibition of RNA or protein synthesis. JImmunol, 1990; 145:1859 - 1867
  • 7Falcieri E, Gobbi P, Cataldi A, et al. Nuclear pores in the apoptotic cell.Histochem J, 1994; 26:754 - 763
  • 8Perkins C, Kim CN, Fang G, et al. Arsenic inducss apoptosis of multidrug-resistanthuman myeloid leukemia cells that express BcrAbl or overexpress MDR, MRP, Bcl-2, orBel-x(L). Blood, 2000;95:1014 - 1022
  • 9Larochette N, Decaudin D, Jacotot E, et al. Arsenite induces apoptosis via a directeffect on the mitochondrial permeability transition pore. Exp Cell Res, 1999; 249:413- 421
  • 10Chen YC, Lin-Shian SY, Lin JK. Involvement of reactive oxygen species and caspase3 activation in arsenite-induced apoptosis. J Cell Physiol, 1998; 177:324- 333

同被引文献30

引证文献3

二级引证文献8

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