ATO,ATRA/G-CSF联合使用加速RAR α降解诱导NB4细胞末端分化  

ATO in Combination with ATRA /G-CSF Inducing Terminal Differentiation of NB4 Cells by Accelerated RAR α Degradation

作　　者：马玲[1] 刘宇鹏[1] 王滨有[1] 李海霞[1] 杨晓蕾[1] 董均明 

机构地区：[1]哈尔滨医科大学公共卫生学院,黑龙江哈尔滨150081

出　　处：《中医药学报》2013年第6期51-53,共3页Acta Chinese Medicine and Pharmacology

基　　金：黑龙江省教育厅海外学人资助项目(1154h20);黑龙江省教育厅科技研究项目资助

摘　　要：目的:探讨三氧化二砷(ATO)、全反式维甲酸(ATRA)及粒细胞集落刺激因子(G-CSF)(A/G)联合使用,诱导NB4细胞末端分化的分子机理。方法:台盼蓝染色记录细胞生长,吉姆萨染色观察细胞的形态学变化,流式细胞仪分析确定细胞分化分子标志及凋亡,Western blot观察RAR α蛋白的表达。结果:NB4细胞经过ATO+A/G处理,出现形态学末端分化特征和免疫表型的成熟。Western blot结果显示,RAR α基因是ATO特定的靶向目标。结论:ATO联合ATRA/G-CSF能够诱导NB4细胞末端分化,其机理与调节RAR α的表达有关。Abstract： Objective ： To investigate the molecular mechanism of ATO in combination with ATRA/G - CSF （A/G） in- duced terminal differentiation of NB4 cells. Methods ：Trypan blue staining was used to record cells growth, Cell morpho- logical features were observed by Giemsa staining, molecular marker of cell differentiation and cell apoptosis were deter- mined by flow cytometry （ FCM）, the expression of RARct was detected by Western blot. Results ： NB4 cells present the morphological terminal differentiation and the immune phenotype maturation treated by ATO ＋ A/G. Western blot results showed that RAR α gene was the specific goal. Conclusion：ATO combined with A/G could induce terminal differentia- tion of NB4 cells, and its mechanism is related to the regulation of RAR of expression.

关 键 词：三氧化二砷(ATO) 全反式维甲酸(ATRA) 粒细胞集落刺激因子(G-CSF) 末端分化 RAR伐 

分 类 号：R285.5[医药卫生—中药学]