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

晁荣; 靳蕊蕊; 陈彻; 席亚明; 楚惠媛; 李明; 张豪

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

更新时间：2026-01-09

- Emodin induces apoptosis and down-regulates Bcl-2/Bax in leukemia KG-1a cells
- Journal of Army Medical University Vol. 34, Issue 13, Pages: 1297-1299(2012)
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  CLC： R285.5;R73-361;R733.7
- Published：2012
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晁荣,靳蕊蕊,陈彻,席亚明,楚惠媛,李明,张豪.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[J].陆军军医大学学报(原第三军医大学学报),2012,34(13):1297-1299.

　Chao Rong,Jin Ruirui,Chen Che,Xi Yaming,Chu Huiyuan,Li Ming,Zhang Hao.Emodin induces apoptosis and down-regulates Bcl-2/Bax in leukemia KG-1a cells[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(13):1297-1299.
晁荣,靳蕊蕊,陈彻,席亚明,楚惠媛,李明,张豪.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[J].陆军军医大学学报(原第三军医大学学报),2012,34(13):1297-1299. DOI：

　Chao Rong,Jin Ruirui,Chen Che,Xi Yaming,Chu Huiyuan,Li Ming,Zhang Hao.Emodin induces apoptosis and down-regulates Bcl-2/Bax in leukemia KG-1a cells[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(13):1297-1299. DOI：

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(IC

)约为171.8 μmol/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G

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。

Abstract

Objective To determine the effect of emodin on the proliferation and apoptosis in human acute myeloid leukemia cell line KG-1a

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

100 and 200 mol/L. Cell viability was measured with MTT 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-1a cells

with IC

value of 171.8 μmol/L after treatment for 48 h. Emodin blocked cell cycle at G

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-1a cells

which might be related to the down-regulation of Bcl-2 and up-regulation of Bax.

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