The mechanism of <sup>131</sup>I-GM-CSF inducing apoptosis of HL-60/ADM cells

ZHANG Ping; et al

doi:10.13406/j.cnki.cyxb.2005.05.006

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The mechanism of ¹³¹I-GM-CSF inducing apoptosis of HL-60/ADM cells

更新时间：2024-01-17

- The mechanism of ¹³¹I-GM-CSF inducing apoptosis of HL-60/ADM cells
- Journal of Chongqing Medical University Issue 5, (2005)
- 作者机构：
  
  1. 重庆医科大学附属第二医院血液科
  2. 重庆医科大学附属第二医院血液科,重庆,400010
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2005.05.006
  CLC： R733.7
- Published：2005，
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[1]张萍,娄世锋,周慷.~(131)I-GM-CSF诱导HL-60/ADM细胞凋亡机制研究[J].重庆医科大学学报,2005(05):26-28+33.

ZHANG Ping, et al. The mechanism of ¹³¹I-GM-CSF inducing apoptosis of HL-60/ADM cells. [J]. Journal of Chongqing Medical University (5).(2005)
[1]张萍,娄世锋,周慷.~(131)I-GM-CSF诱导HL-60/ADM细胞凋亡机制研究[J].重庆医科大学学报,2005(05):26-28+33. DOI： 10.13406/j.cnki.cyxb.2005.05.006.

ZHANG Ping, et al. The mechanism of ¹³¹I-GM-CSF inducing apoptosis of HL-60/ADM cells. [J]. Journal of Chongqing Medical University (5).(2005) DOI： 10.13406/j.cnki.cyxb.2005.05.006.

摘要

目的:研究131I-GM-CSF诱导HL-60/ADM细胞凋亡机制。方法:采用体外放射免疫治疗模型

通过透射电子显微镜、流式细胞术及免疫细胞化学检测等方法

研究131I-GM-CSF辐射一定时间后HL-60/ADM细胞的凋亡率、凋亡形态学上的改变、相关基因的表达和线粒体膜电位的改变。结果:显示131I-GM-CSF可诱导HL-60/ADM细胞凋亡

在诱导细胞凋亡过程中

HL-60/ADM细胞超微结构明显破坏

细胞线粒体膜电位降低

Bax表达上调

Bcl-2、Bcl-xl表达下调。结论:131I-GM-CSF作为放射导向治疗药物能诱导HL-60/ADM细胞凋亡

具有抗白血病的作用

其诱导凋亡的机制与开放线粒体膜的通透性转换孔（MPT）、降低线粒体膜电位（MTP）

上调Bax

下调Bcl-2、Bcl-xl有关。

Abstract

Objective:To investigate the mechanism of

131

I-GM-CSF inducing apoptosis of HL-60/ADM cells.Methods:An in vitro radioimmunotherapy（RAIT） model was employed.Data were collected from transmission electrion microscopy

flow cytometric analysis and immunocytochemistry assay.Results:After exposure to

131

I-GM-CSF

HL-60/ADM cells were induced to apoptosis.The cell mitochondrial transmembrane potential（MTP） reduced and HL-60/ADM cells appeared the classical apoptotic morphology.The Bax was up regulated

while Bcl-2 and Bcl-xl was decreased.Conclusion:

131

I-GM-CSF can induce HL-60/ADM apoptosis through opening the mitochondrial permeability transition pore and reducing MTP

which suggests that

131

I-GM-CSF may be available in therapy of AML.

关键词

131I-GM-CSF细胞凋亡放射导向治疗线粒体膜电位

Keywords

131I-GM-CSFcell apoptosisTargeted radiopharmaceutic therapyMitochondrial transmembrane potential

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⁰

The mechanism of 131I-GM-CSF inducing apoptosis of HL-60/ADM cells

DOI：10.13406/j.cnki.cyxb.2005.05.006

摘要

Abstract

关键词

Keywords

references

The mechanism of ¹³¹I-GM-CSF inducing apoptosis of HL-60/ADM cells