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丹参酮ⅡA诱导白血病细胞凋亡过程中端粒酶活性的改变
引用本文:宋毅,袁淑兰,羊裔明,王修杰,黄光琦. 丹参酮ⅡA诱导白血病细胞凋亡过程中端粒酶活性的改变[J]. 中国中药杂志, 2005, 30(3): 207-211
作者姓名:宋毅  袁淑兰  羊裔明  王修杰  黄光琦
作者单位:四川大学华西医院 四川成都610041(宋毅,袁淑兰,羊裔明,王修杰),四川大学华西医院 四川成都610041(黄光琦)
基金项目:卫生部科研基金资助项目(961240)
摘    要:目的观察丹参酮ⅡA(TanⅡA)对HL60,K562细胞端粒酶活性的抑制作用和对凋亡相关基因的影响,探讨丹参酮ⅡA对造血细胞的作用机理。方法以HL60,K562为靶细胞,应用细胞培养技术,流式细胞术,透射电镜观察TanⅡA对HL60,K562细胞的作用,利用PCRTRAP方法检测TanⅡA处理前后HL60,K562细胞端粒酶活性的改变。结果经05μg·mL-1TanⅡA作用6d后,HL60,K562细胞生长明显受到抑制,生长抑制率分别为756%和563%。经丹参酮诱导后,HL60,K562细胞发生凋亡,出现亚二倍体峰;同时显著下调HL60及K562细胞的cmyc,bcl2基因表达,上调cfos基因表达。HL60,K562细胞在TanⅡA作用后,端粒酶活性受到抑制,端粒酶活性抑制率分别为308%,508%。结论TanⅡA可明显抑制HL60和K562细胞的增殖和细胞端粒酶活性,并诱导细胞凋亡。

关 键 词:丹参酮ⅡA  白血病细胞株  端粒酶  凋亡
文章编号:1001-5302(2005)03-0207-05
收稿时间:2004-04-29

Alteration of activities of telomerase in tanshinone IIA inducing apoptosis of the leukemia cells]
SONG Yi;YUAN Shu-lan;YANG Yi-ming;WANG Xiu-jie;HUANG Guang-qi. Alteration of activities of telomerase in tanshinone IIA inducing apoptosis of the leukemia cells][J]. China Journal of Chinese Materia Medica, 2005, 30(3): 207-211
Authors:SONG Yi  YUAN Shu-lan  YANG Yi-ming  WANG Xiu-jie  HUANG Guang-qi
Affiliation:West China Hospital, Sichuan University, Chengdu 610041, China.
Abstract:OBJECTIVE: To investigate the effect of tanshinone IIA on HL-60 and K562 cells apoptosis, and to assay the inhibition of the telomerase activities in the leukemia cell apoptosis induced by Tanshinone. METHOD: Using the techniques of cell culture in vitro, flow cytometry and PCR-TRAP observed the telomerase activities and apoptosis of HL-60 and K562 cells which treated by Tan IIA. RESULT: 0.5 microg x mL(-1) Tan IIA could obviously inhibit HL-60 and K562 cell lines growth (P < 0.05), down-regulate c-myc, bcl-2 gene and up-regulate c-fos and p53 gene expression as well as induce leukemia cell apoptosis, the apoptotic rates of HL-60 and K562 cells were 11.8% and 21.8% respectively. The telomerase activities significant decreased, the inhibiting rates in HL60 and K562 cells were 30.8% and 50.8% respectively. CONCLUSION: Tan IIA could significantly inhibit the proliferation and telomerase activities of HL-60 and K562 cells and induce the leukemia cell apoptosis.
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