The investigation of the proliferation inhibition and apoptosis of K562 ninduced by dexamethasone

LIU Chang; et al

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The investigation of the proliferation inhibition and apoptosis of K562 ninduced by dexamethasone

更新时间：2024-01-17

- The investigation of the proliferation inhibition and apoptosis of K562 ninduced by dexamethasone
- Journal of Chongqing Medical University Issue 8, Pages: 911-913(2008)
- 作者机构：
  
  重庆医科大学医学检验系教育部重点实验室
- 作者简介：
- 基金信息：
- DOI：
  CLC： R733.7
- Published：2008，
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[1]刘畅,金丹婷,钟梁,刘北忠,王东生,郝坡,王翀,王春光.地塞米松对K562细胞增殖抑制作用及诱导凋亡机制的研究[J].重庆医科大学学报,2008(08):911-913+979.

LIU Chang, et al. The investigation of the proliferation inhibition and apoptosis of K562 ninduced by dexamethasone. [J]. Journal of Chongqing Medical University (8):911-913(2008)
[1]刘畅,金丹婷,钟梁,刘北忠,王东生,郝坡,王翀,王春光.地塞米松对K562细胞增殖抑制作用及诱导凋亡机制的研究[J].重庆医科大学学报,2008(08):911-913+979. DOI：

LIU Chang, et al. The investigation of the proliferation inhibition and apoptosis of K562 ninduced by dexamethasone. [J]. Journal of Chongqing Medical University (8):911-913(2008) DOI：

摘要

目的:研究地塞米松对K562细胞的增殖抑制作用及诱导细胞凋亡的机制。方法:用不同浓度的地塞米松对K562细胞进行处理

检测细胞增殖抑制率

观察细胞凋亡的形态学变化

测定细胞端粒酶活性

Fas表达及NO产生情况。结果:地塞米松能抑制K562细胞的增殖

降低端粒酶活性

使Fas表达上调

诱导细胞凋亡。但对NO的生成不具有显著性差异。结论:地塞米松可能通过抑制端粒酶的活性而诱导K562细胞的凋亡。同时

Fas也可能参与了凋亡的调节。

Abstract

Objective:To investigate the effect of dexamethasone on the growth and the mechanism of apoptosis in K562 cells.Methods:Treat of different dosages of dexamethasone in K562 cell cultural to observe cell inhibitory rate and cell morphology variation.To detected telomerase activity

Fas expression and NO release.Results:Dexamethasone can inhibit the proliferation of K562 cell

decrease telomerase activity

increase Fas expression and induce apoptosis.But no significant effect on nitric oxide production.Conclusion:Inhibit telomerase activity and increase Fas expression maybe one of mechanism of apoptosis.

关键词

地塞米松凋亡端粒酶K562细胞

Keywords

dexamethasoneapoptosistelomeraseK562 cell

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