文献类型：期刊文献

中文题名：大黄素诱导白血病KG-1a细胞凋亡及对Bcl-2/Bax mRNA表达的影响

英文题名：Emodin induces apoptosis and down-regulates Bcl-2/Bax in leukemia KG-1a cells

作者：晁荣[1];靳蕊蕊[1];陈彻[2];席亚明[1];楚惠媛[2];李明[1];张豪[1]

第一作者：晁荣

机构：[1]兰州大学第一医院血液科,血液学研究所;[2]甘肃中医学院医学基础实验教学中心

第一机构：兰州大学第一医院血液科,血液学研究所

年份：2012

卷号：34

期号：13

起止页码：1297

中文期刊名：第三军医大学学报

外文期刊名：Journal of Third Military Medical University

收录：CSTPCD;;北大核心:【北大核心2011】；CSCD:【CSCD2011_2012】；

基金：甘肃省财政厅基本科研业务费专项资金{甘政财[2010]176号};2011年甘肃省普通中医药科研立项资助课题(GZK-2011-69)~~

语种：中文

中文关键词：大黄素;KG-1a细胞;Bcl-2;Bax;细胞凋亡;干细胞

外文关键词：emodin ; KG-1 a cells ; Bcl-2 ; Bax; cell apoptosis ; stem cells

摘要：目的本研究观察大黄素(emodin)对人急性髓系白血病KG-1a细胞的增殖及凋亡影响,探讨Bcl-2/Bax基因在其中的作用。方法采用四唑蓝比色试验(MTT)检测大黄素对KG-1a细胞增殖的影响;流式细胞术(FCM)测定细胞周期变化与凋亡情况;RT-PCR法检测大黄素作用后细胞Bcl-2/Bax mRNA表达的变化。结果大黄素能抑制KG-1a细胞的增殖,作用48 h的半数抑制浓度(IC50)约为171.8μmol/L流式细胞仪分析出现典型的亚二倍体峰(凋亡峰),将细胞阻滞于G0/G1期,大黄素作用后KG-1a细胞Bcl-2基因表达下调,而Bax基因表达上调,并呈量效关系。结论大黄素可诱导KG-1a细胞凋亡,其机制可能与下调Bcl-2,上调Bax基因表达水平有关。
Objective To determine the effect of emodin on the proliferation and apoptosis in human emia cell line KG-1 a, and to investigate the role of Bcl-2/Bax in the process. Methods KG-1a cells were exposed to emodin at the doses of 25, 50, 100 and 200 mol/L. Cell viability was measured with MTY assay. The change of cell cycle and apoptosis were detected by flow cytometry （FCM）. The expression of Bcl-2/Bax mRNA was assessed by RT-PCR. Results Emodin significantly inhibited the proliferation in KG-1 a cells, with IC50 value of 171.8 μmol/L after treatment for 48 h. Emodin blocked cell cycle at G0/G1 phase, and a remarkable sub-G1 apoptotic peak was observed according to the detection of flow cytometry. The expression of Bcl-2 was down-regulated, while that of Bax was obviously up-regulated in a dose-dependent manner. Conclusion Emodin can significantly induce apoptosis of KG-1 a cells, which might be related to the down-regulation of Bcl-2 and up-regulation of Bax.