Bisdemethoxycurcumin Induced Human Leukemia K562 Cells Apoptosis Through Down-regulation of Mitochondrial Membrane Potential

MIAO Jiu-wang; ZHANG Qin-de; WANG Hong-bo; FU Feng-hua

doi:10.13422/j.cnki.syfjx.2015240109

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Bisdemethoxycurcumin Induced Human Leukemia K562 Cells Apoptosis Through Down-regulation of Mitochondrial Membrane Potential

更新时间：2024-09-23

- Bisdemethoxycurcumin Induced Human Leukemia K562 Cells Apoptosis Through Down-regulation of Mitochondrial Membrane Potential
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 21, Issue 24, Pages: 109-113(2015)
- 作者机构：
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- DOI：10.13422/j.cnki.syfjx.2015240109
  CLC： R285
- Published：2015
- 稿件说明：
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MIAO Jiu-wang, ZHANG Qin-de, WANG Hong-bo, et al. Bisdemethoxycurcumin Induced Human Leukemia K562 Cells Apoptosis Through Down-regulation of Mitochondrial Membrane Potential[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(24): 109-113.
DOI：

MIAO Jiu-wang, ZHANG Qin-de, WANG Hong-bo, et al. Bisdemethoxycurcumin Induced Human Leukemia K562 Cells Apoptosis Through Down-regulation of Mitochondrial Membrane Potential[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(24): 109-113. DOI： 10.13422/j.cnki.syfjx.2015240109.

摘要

目的:探讨双去甲氧基姜黄素对K562细胞增殖的影响及其机制。方法:以1

100μmol·L-1的双去甲氧基姜黄素对K562细胞作用48 h或72 h后MTT法检测细胞增殖;以10

50μmol·L-1的双去甲氧基姜黄素对K562细胞作用24 h或48 h实验

另设空白组

AO/EB双染法倒置荧光显微镜观察凋亡形态

Rh123染色流式细胞仪检测线粒体膜电位

Annxin V/PI染色流式细胞仪检测凋亡率

Westren blot方法检测Bcl-2

Bax的表达活性。结果:与空白组比较

双去甲氧基姜黄素可剂量依赖性抑制K562细胞的增殖

在30

50μmol·L-1浓度下

双去甲氧基姜黄素可诱导细胞凋亡

下调Bcl-2/Bax

并可降低线粒体的膜电位(P<0.01)。结论:双去甲氧基姜黄素可抑制K562细胞的增殖

作用机制可能与改变线粒体膜电位诱导的细胞凋亡有关。

Abstract

Objective: To explore the antitumor effects and mechanisms of bisdemethoxycurcumin(BDMC) on K562 cells. Method: K562 cells were treated with 1

100μmol·L-1 of BDMC for 48 h or 72 h

then the anti-proliferative effect was assessed by MTT assay.K562 cells were treated with 10

50μmol·L-1 of BDMC for 24 h or 48 h

and another blank group was also established. The apoptosis morphology was observed by AO/EB staining using fluorescence microscope

mitochondrial membrane potential(MMP) was detected by Rhodamine 123 staining using flow cytometry instrument and apoptosis rate was detected by Annexin V/PI staining using flow cytometry instrument. The expression of Bcl-2

Bax was evaluated by Western blot method. Result: BDMC could inhibit the proliferation of K562 cells in a dose dependent manner when compared with the blank group. BDMC at the dose of 30

50μmol·L-1 could induce cell apoptosis

decrease the ratio of Bcl-2/Bax and reduce mitochondrial membrane potential. Conclusion: BDMC could inhibit proliferation of K562 cells

and its mechanism may be related with the induction of cell apoptosis via mitochondria pathway.

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