摘要
目的:了解氧化砷(As2O3)治疗急性早幼粒细胞白血病(APL)的细胞和分子机制。方法:以早幼粒细胞白血病细胞株NB4细胞等为研究对象,利用流式细胞仪,DNA电泳,Northern、Western印迹,免疫组化等手段,观察As2O3对APL的作用。结果:As2O3能显著诱导NB4细胞凋亡,而不影响HL-60和U937的生长和存活。氧化砷能有效降低NB4细胞中bcl-2基因的表达,而对其它几种凋亡相关基因(包括p53、c-myc、bax和bcl-XL)的mRNA水平无影响。结论:这可能是As2O3诱导NB4细胞凋亡的分子机制之一。
Objective:To illustrate the possible cellular and molecular mechanisms of arsenic trioxide(As 2 O 3 ) in the treatment of acute promyelocytic leukemia(APL).Methods:APL cell line NB4 was used for in vitro studies.The effect of As 2O 3 on APL was studied by using flow cytometry, DNA electrophoresis, Narthern blotting and Western blotting. Results:As 2O 3 induced NB4 cell apoptosis ,while not inhibiting the growth and survival of two other leukemic cell lines (HL 60 and U937).Furthermore,As 2O 3 effectively down regulated the expression of bcl 2 gene without changing the mRNA levels of other apoptosis associated genes (including p53,c myc,bax and bcl XL).Conclusion: These might be one of the molecular mechanisms of As 2O 3 induced NB4 cell apoptosis.
出处
《中华血液学杂志》
CAS
CSCD
北大核心
1997年第1期25-28,共4页
Chinese Journal of Hematology
基金
国家自然科学基金
卫生部优秀青年人才基金
上海市科委基金
上海市科技启明星计划
上海血液学研究所胡应洲基金