<sup>131</sup>I-GM-CSF induced apoptosis of HL-60

ZHOU Kang; et al

doi:10.13406/j.cnki.cyxb.2005.03.011

您当前的位置：

首页 >

文章列表页 >

¹³¹I-GM-CSF induced apoptosis of HL-60

更新时间：2024-01-17

- ¹³¹I-GM-CSF induced apoptosis of HL-60
- Journal of Chongqing Medical University Issue 3, Pages: 348-351(2005)
- 作者机构：
  
  1. 重庆医科大学第二临床学院血液科
  2. 重庆医科大学第二临床学院血液科,重庆,400010
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2005.03.011
  CLC： R733.71
- Published：2005，
扫描看全文
[1]周慷,娄世锋,张萍.~(131)I-GM-CSF诱导HL-60细胞凋亡机制的体外研究[J].重庆医科大学学报,2005(03):348-351.

ZHOU Kang, et al. ¹³¹I-GM-CSF induced apoptosis of HL-60. [J]. Journal of Chongqing Medical University (3):348-351(2005)
[1]周慷,娄世锋,张萍.~(131)I-GM-CSF诱导HL-60细胞凋亡机制的体外研究[J].重庆医科大学学报,2005(03):348-351. DOI： 10.13406/j.cnki.cyxb.2005.03.011.

ZHOU Kang, et al. ¹³¹I-GM-CSF induced apoptosis of HL-60. [J]. Journal of Chongqing Medical University (3):348-351(2005) DOI： 10.13406/j.cnki.cyxb.2005.03.011.

摘要

目的:观察131I-GM-CSF诱导HL-60细胞凋亡及其机制

探讨其在急性髓系白血病放射导向治疗中的作用。方法:采用MTT法、TUNEL、透射电子显微镜研究131I-GM-CSF辐射后HL-60细胞的存活率、凋亡率和形态的改变;用流式细胞术和免疫细胞化学方法检测线粒膜电位的改变以及凋亡相关基因的表达。结果:放射性浓度≥18.5×108Bq/L时HL-60细胞存活率显著下降。131I-GM-CSF能致HL-60细胞凋亡、超微结构破坏、线粒体膜电位降低。在诱导细胞凋亡过程中

p53表达上调

bcl-2、bcl-xl表达下调。结论:GM-CSF作为载体携带131I能诱导HL-60细胞凋亡

具有抗白血病的作用。其诱导凋亡的机制与上调p53

下调bcl-2、bcl-xl

开放线粒体膜的通透性转换孔

降低线粒体膜电位有关。

Abstract

Objective:To investigate the effect and mechanism of apoptosis of HL-60 cells induced by 131 I-GM-CSF.Methods:The relevant data were collected from tetrazolium microculture(MTT)cellular cytotoxicity test

TUNEL technology

transmission electron microscopy

flow cytometric analysis and immunocytochemistry assay.Results:When the radioative dose was higher than 18.5×108Bq/L

cell survival rate was markedly decreased.Cell apoptosis rate was significantly increased and cellular ultrastructure was markedly destroyed by 131 I-GM-CSF.Loss of mitochondrial transmembrane potential(MTP) was found in cells treated with 131 I-GM-CSF.The p53 expression was up regulated

while those of bcl-2 and bcl-xl were decreaded.Conclusion:These results show that 131 I-GM-CSF can induce significant apoptosis of HL-60 by opening the mitochondrial permeability transition pore and reducing MTP

which suggests that 131 I-GM-CSF may be available in treatment of AML.

关键词

细胞凋亡放射导向治疗白血病

Keywords

apoptosisTargeted radiopharmaceutical therapyleukemia

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Growth-inhibiting effects of oxaliplatin on K562 cells in vitro

Effect of Glycyrrhiza uralensis Fisch. endophytes combined with cisplatin on proliferation and apoptosis of A549 cells

Milk fat globule-EGF factor Ⅷ attenuates apoptosis and permeability damage of the intestinal mucosa in rats with obstructive jaundice

Effect of andrographolide on TBHP-induced apoptosis of intervertebral disc nucleus pulposus cells and its mechanism

Factors affecting the quality of life in children with leukemia and the relevant research progress at home and abroad

Related Author

CHEN Shu

et al

娄世锋

Zhang Shanglong

Zhang Nan

Lian Xiaolong

Ye Liqiao

Ma Quhuan

Related Institution

重庆医科大学病理生理教研室

College of Pharmacy，Gansu University of Chinese Medicine

Department of Hepatobiliary Pancreatic Surgery,Daping Hospital,Army Medical University

Department of Hepatobiliary Pancreatic Surgery,People’s Hospital of Chongqing Liang Jiang New Area

⁰

131I-GM-CSF induced apoptosis of HL-60

DOI：10.13406/j.cnki.cyxb.2005.03.011

摘要

Abstract

关键词

Keywords

references

¹³¹I-GM-CSF induced apoptosis of HL-60