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Bcl-2基因反义核酸增强三氧化二砷对NB4细胞凋亡效应
引用本文:沈伟利,张洹.Bcl-2基因反义核酸增强三氧化二砷对NB4细胞凋亡效应[J].中国病理生理杂志,2001,17(7):618-621.
作者姓名:沈伟利  张洹
作者单位:暨南大学医学院血液病研究所, 广东广州 510632
基金项目:广东省自然科学基金资助项目(No.980710);国家自然科学基金资助项目(No.39870361)
摘    要:目的:研究和探索bcl-2基因反义核酸(bcl-2ASODN)是否能提高三氧化二砷(As2O3)对NB4白血病细胞的凋亡效应。方法:采用微量细胞培养的方法,观察反义核酸、砷剂单独以及反义核酸、砷剂联合培养NB4细胞的生物效应和凋亡形态变化;用免疫组化的方法,结合流式细胞技术,测定NB4细胞的DNA和Bcl-2蛋白的变化。结果:As2O3(0.25μmol/L)+bcl-2ASODN(10.0μmol/L)联合诱导NB4细胞凋亡作用显著强于单用As2O3(0.25μmol/L)或bcl-2ASODN(10.0μmol/L)(P<0.01)。流式细胞仪检测显示,联合用药Bcl-2蛋白表达亦明显少于反义核酸、砷剂单独给药组(P<0.01)。结论:bcl-2基因反义核酸能明显提高和显著增强As2O3对NB4白血病细胞的致凋亡效应。

关 键 词:寡核苷酸类  反义  基因  bcl-2  凋亡  
文章编号:1000-4718(2001)07-0618-04
收稿时间:2000-10-09
修稿时间:2000年10月9日

The antisense phosphorothioate oligodeoxynucleotides of bcl-2 oncogene enhances the apoptotic effect of As_2O_3 on NB4 leukemic cells
SHEN Wei-li,ZHANG Yuan.The antisense phosphorothioate oligodeoxynucleotides of bcl-2 oncogene enhances the apoptotic effect of As_2O_3 on NB4 leukemic cells[J].Chinese Journal of Pathophysiology,2001,17(7):618-621.
Authors:SHEN Wei-li  ZHANG Yuan
Institution:Institute of Hematology, Medical College of Jinan University, Guangzhou 510632, China
Abstract:AIM: To study and explore whether the antisense phosphorothioate oligodeoxynucleotides (ASODN) of bcl-2 oncogene would increase the apoptotic effect of As2O3 on NB4 leukemic cells. METHODS: The biological and morphological changes in NB4 cells from microculture with As2O3, bcl-2 ASODN or both were observed. The changes in DNA content and Bcl-2 protein of NB4 cells from microculture with As2O3, bcl-2 ASODN or both were determined by tissue chemistry and flowcytometry. RESULTS: There was much more apoptotic effect of As2O3 on NB4 cells while it combined with bcl- 2 ASODN (ASODN 10.0 μmol/L+ As2O3 0.25 μmol/L) than alone(ASODN 10.0 μmol/L or As2O3 0.25μmol/L),and so did inhibitory effect of Bcl-2 protein expression by flow cytometry. CONCLUSION:The bcl-2 ASODN can enhance the apoptotic effect of As2O3 on NB4 leukemic cells.
Keywords:Oligonucleotides  antisense  Genes  bcl-2  Apoptosis
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