Shikonin Induce K562 Cell Apoptosis through Oxidative Stress

RAN Fang; JIANG Jiang-tao; ZHAO Hong; YANG Xin-hui; ZHANG Bo; WANG Zhen-hua; ZHENG Qiu-sheng

doi:10.11653/syfj2013130221

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Shikonin Induce K562 Cell Apoptosis through Oxidative Stress

更新时间：2024-01-04

- Shikonin Induce K562 Cell Apoptosis through Oxidative Stress
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 19, Issue 13, Pages: 221-225(2013)
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- DOI：10.11653/syfj2013130221
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- Published：2013
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RAN Fang, JIANG Jiang-tao, ZHAO Hong, et al. Shikonin Induce K562 Cell Apoptosis through Oxidative Stress[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(13): 221-225.
DOI：

RAN Fang, JIANG Jiang-tao, ZHAO Hong, et al. Shikonin Induce K562 Cell Apoptosis through Oxidative Stress[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(13): 221-225. DOI： 10.11653/syfj2013130221.

摘要

目的: 研究紫草素(shikonin)诱导人红白血病细胞(K562)凋亡作用并初步探讨其机制。方法: 噻唑蓝(thiazolyl blue

MTT)染色法检测紫草素对K562细胞的增殖抑制作用;Hoechst 33258和吖啶橙(acridine orange

AO)/溴化乙啶(ethidium bromide

EB)染色法观察细胞凋亡形态;反转录酶-聚合酶链锁反应(reverse transcription-polymerase chain reaction

RT-PCR)法检测与凋亡相关基因:B细胞淋巴因子基因2相关X蛋白(B-cell lymphoma gene 2 associated X protein

Bax)、B细胞淋巴因子基因2同源3结构域相互作用基团死亡促进因子(BH3 interacting domain death agonist

Bid)、B细胞淋巴因子基因xL(B-cell lymphoma gene xL

Bcl-xL)、p53上调凋亡调控因子(p53 up-regulated modulator of apoptosis

PUMA)、B细胞淋巴因子基因2同源拮抗因子(B-cell lymphoma gene 2 homologous antagonist

Bak)、B细胞淋巴因子-w(B-cell lymphoma-w

Bcl-w)、B细胞淋巴因子基因2相关死亡促进因子(B-cell lymphoma gene 2 associated death promoter

Bad)信使核糖核酸(Messenger RNA

mRNA)表达的变化;荧光染料二乙酸-2'

7'-二氯荧光素盐(oxalic acid-2'

7'-dichlorofluorescein

DCFHDA)分析细胞内总活性氧(Reactive Oxygen Species

ROS)的变化;荧光染料5-氯甲基二已酸荧光素(5-chloromethylfluorescein diacetate

CMFDA)分析细胞内还原型谷胱甘肽(reduced glutathione hormone

GSH)含量的变化。结果: ①0.2~1.6 mg·L-1的紫草素对K562细胞增殖呈浓度依赖性抑制;②0.2~0.5 mg·L-1的紫草素处理组细胞出现明显凋亡特征;③0.2~0.5 mg·L-1的紫草素处理组促凋亡蛋白Bid

Bad

Bak

PUMA

Bax的mRNA表达显著增加

抑制凋亡蛋白Bcl-w和Bcl-xL的mRNA表达明显下调;④0.2~0.5 mg·L-1的紫草素处理组

细胞内总活性氧含量升高

还原型谷胱甘肽含量降低。结论: 紫草素有较强的抑制K562细胞增殖并诱导其凋亡的作用

该过程伴随细胞内氧化还原状态的改变

紫草素诱导的K562细胞的凋亡与细胞内氧化胁迫有关。

Abstract

Objective:Tostudy the mechanism of shikonin inducing K562 cells apoptosis. Method: MTT colorimetric assay was used to examine the proliferation inhibition of shikonin on K562 cells. Hoechst 33258 and acridine orange(AO)/ethidium bromide(EB) fluorescent staining were used to observe the morphological changes of apoptotic cell. The mRNA expression levels of B-cell lymphoma gene 2 associated X protein(Bax)

BH3 interacting domain death agonist(Bid)

B-cell lymphoma gene xL(Bcl-xL)

p53 up-regulated modulator of apoptosis(PUMA)

B-cell lymphoma gene 2 homologous antagonist(Bak)

B-cell lymphoma-w(Bcl-w) and B-cell lymphoma gene 2 associated death promoter(Bad) were detected using RT-PCR analysis. The changes of reactive oxygen species(ROS) and reduced GSH were detected using molecular probe DCFHDA and CMFDA:CMFDA

separately. Result: Shikonin(0.2-1.6 mg·L-1)inhibited K562 cell proliferation in concentration-dependent manner

and induced cell apoptosis. Typical apoptotic changes were observed in K562 cells under the shikonin(0.2-0.5 mg·L-1) treatment groups. The expression of proapoptotic protein (Bid

Bad

Bak

PUMA

Bax) was increased and antiapoptotic protein (Bcl-w

Bcl-xL) decreased. ROS formation increased

but reduced glutathione level was decreased. Conclusion: Shikonin can inhibite K562 cell proliferation and induce apoptosis through inducing oxidative stress.

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