Effect of artesunate on autophagy of leukemic K562 cells and its mechanism

Zhang Ping; Yang Guicun; Chen Hongxia; Wang Xiaojing; Liang Shaoyan; Xu Youhua

doi:10.13406/j.cnki.cyxb.001097

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Effect of artesunate on autophagy of leukemic K562 cells and its mechanism

更新时间：2024-01-17

- Effect of artesunate on autophagy of leukemic K562 cells and its mechanism
- Journal of Chongqing Medical University Vol. 42, Issue 11, Pages: 1457-1461(2017)
- 作者机构：
  
  重庆医科大学附属儿童医院血液科儿童发育疾病研究教育部重点实验室儿童发育重大疾病国家国际科技合作基地儿科学重庆市重点实验室
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.001097
  CLC： R733.7
- Published：2017，
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Zhang Ping, Yang Guicun, Chen Hongxia, et al. Effect of artesunate on autophagy of leukemic K562 cells and its mechanism. [J]. Journal of Chongqing Medical University 42(11):1457-1461(2017)
DOI：

Zhang Ping, Yang Guicun, Chen Hongxia, et al. Effect of artesunate on autophagy of leukemic K562 cells and its mechanism. [J]. Journal of Chongqing Medical University 42(11):1457-1461(2017) DOI： 10.13406/j.cnki.cyxb.001097.

摘要

目的:研究青蒿琥酯(artesunate

ART)对白血病K562细胞自噬的影响

并初步探讨其作用机制。方法:不同浓度(0、6.25、12.5、25、50、100 mg/L)ART刺激K562细胞

用CCK-8法分别检测24、48、72 h后K562细胞和健康人外周血有核细胞的增殖抑制情况

并计算48 h半数抑制浓度(inhibitory concentration

IC50);IC50浓度下

采用CCK-8法、Annexin V-FITC/PI双染法联合流式细胞仪分别检测空白对照组(未加药物)、10μmol/L自噬抑制剂二磷酸氯喹(chloroquine diphosphate

CQ)组、30 mg/L ART+10μmol/L CQ组及30 mg/L ART组K562细胞的增殖抑制率、凋亡率;Western blot检测不同浓度ART作用K562细胞48 h

及IC50浓度下ART作用K562细胞12、24、48、72 h后

LC3、p62、HMGB1、Beclin1的蛋白表达情况。结果:ART抑制K562细胞增殖

以时间剂量依赖性方式影响

且作用48 h IC50为30 mg/L;30 mg/L ART+10μmol/L CQ组(70.85±5.57)%的增殖抑制率较30 mg/L ART组(34.07±7.32)%、空白对照组(0.00±2.15)%明显增高;Annexin V-FITC/PI双染法联合流式细胞仪结果显示ART+CQ组(16.67±1.34)%的凋亡率较ART(9.48±1.00)%空白对照组(1.92±0.09)%明显增加;Western blot结果显示

与对照组比较

自噬相关分子LC3、p62的蛋白表达水平在所设定的各浓度及不同干预时间时均上调明显。Beclin1的蛋白表达水平在ART高浓度(25、50、100 mg/L)及干预时间(24、48、72 h)较长时下调明显。HMGB1的蛋白表达水平在ART高浓度(50、100 mg/L)及不同干预时间(12、24、48、72 h)时下调明显。结论:ART以时间剂量依赖性方式抑制K562细胞自噬

可能机制是通过抑制自噬体的融合降解、下调自噬形成相关分子HMGB1、Beclin1的表达而减弱肿瘤细胞对恶劣肿瘤微环境的应激反应、扩大肿瘤细胞的损伤

最终促进K562细胞的死亡。

Abstract

Objective:To study the autophagy of artesunate（ART）on leukemic K562 cells and its possible mechanism. Methods:The inhibitory effect of ART on the proliferation of K562 cells was detected by CCK-8. The cell apoptosis was examined by the flow cy-tometry. Western blot was carried out to detect the expressions of LC3

p62

HMGB1 and Beclin1. Results:ART inhibited the proliferation of K562 cells in a dose-and-time dependent manner

with IC50 value of 30 mg/L at 48 h. In addition

ART could induce the apoptosis of K562 cells and the apoptosis could incease when combined with CQ. According to the results Western blot

ART could up-regulate the expressions of autophagy-related molecule LC3

p62 and down-regulate the expressions of HMGB1

Beclin1. Conclusion:ART shows the effects in inhibiting the autophagy of leukemic K562 cells. Its mechanism may be related to the down-regulation the ex-pression of HMGB1

Beclin1

and the inhibition of autophagic degradation

and that ART-induced inhibition of autophagy may eventually results in the death in K562 cells.

关键词

青蒿琥酯白血病K562自噬

Keywords

artesunateleukemiaK562autophagy

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