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贝母素甲对多药耐药人白血病细胞活力和凋亡的影响及机制

齐彦 廖斌 徐成波 皇甫真萍 陈佳薇

山东医药2017,Vol.57Issue(26):17-20,4.
山东医药2017,Vol.57Issue(26):17-20,4.DOI:10.3969/j.issn.1002-266X.2017.26.005

贝母素甲对多药耐药人白血病细胞活力和凋亡的影响及机制

Effects of peimine on cell viability and apoptosis of multidrug resistant human leukemia cells

齐彦 1廖斌 1徐成波 1皇甫真萍 1陈佳薇1

作者信息

  • 1. 福建中医药大学附属人民医院,福州 350004
  • 折叠

摘要

Abstract

Objective To investigate the effects of peimine on cell viability and apoptosis of multidrug resistant human leukemia K562/A02 cells and the function of reactive oxygen species (ROS) in this progress.Methods The K562/A02 cells were divided into three groups.Cells in the drug group were treated with peimine with the final concentrations of 100, 200, and 400 μmol/L, respectively.Cells in the N acetyl cysteine (NAC) pretreatment group were treated with 5 mmol/L antioxidant NAC, followed by 400μmol/L peimine.Cells in the control group were treated with an equal volume of dissolution medium RPMI1640.The cell viability of each group was detected by MTT, the apoptosis was detected by flow cytometry, and the levels of ROS and glutathione (GSH) in the cells were detected by UV spectrophotometry.Results Compared with the control group, the cell viability of the drug group decreased (P<0.05 or P<0.01), intracellular ROS level increased (P<0.01), GSH concentration decreased (P<0.01), and the apoptosis rate increased (P<0.05).However, the cell viability, the apoptosis rate, and the ROS level in NAC pretreatment group showed no obvious change (all P>0.05).Conclusion Peimine inhibits the cell viability and induces apoptosis of multidrug resistant leukemia K562/A02 cells through inducing the ROS outbreak and thus increasing the GSH content.

关键词

贝母素甲/慢性粒细胞白血病/K562/A02/多药耐药/活性氧/细胞活力/细胞凋亡

Key words

peimine/chronic myeloid leukemia/K562/A02/multidrug resistance/reactive oxygen species/cell viability/apoptosis

分类

医药卫生

引用本文复制引用

齐彦,廖斌,徐成波,皇甫真萍,陈佳薇..贝母素甲对多药耐药人白血病细胞活力和凋亡的影响及机制[J].山东医药,2017,57(26):17-20,4.

基金项目

福建省教育厅中青年教师教育科研项目(JA14161). (JA14161)

山东医药

OACSTPCD

1002-266X

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