1,4-苯醌致K562细胞线粒体功能障碍与凋亡作用

doi:10.3969/j.issn.1004-616x.2017.02.011

癌变·畸变·突变 ›› 2017, Vol. 29 ›› Issue (2): 129-133.doi: 10.3969/j.issn.1004-616x.2017.02.011

1,4-苯醌致K562细胞线粒体功能障碍与凋亡作用

蒋小云, 孙蓉丽, 满招娣, 张娟, 浦跃朴

东南大学公共卫生学院环境医学工程教育部重点实验室, 江苏南京 210009

收稿日期:2017-01-10 修回日期:2017-02-27 出版日期:2017-03-31 发布日期:2017-03-31
通讯作者: 浦跃朴,E-mail:Yppu@seu.edu.cn E-mail:Yppu@seu.edu.cn
作者简介:蒋小云,E-mail:347257066@qq.com。
基金资助:
江苏省普通高校研究生科研创新计划项目（SJZZ15-0024）；国家自然科学基金项目（81373034，81573120）

Induction of mitochondrial dysfunction and apoptosis by 1,4-benzoquinone in K562 cells

JIANG Xiaoyun, SUN Rongli, MAN Zhaodi, ZHANG Juan, PU Yuepu

Key Laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, Jiangsu, China

Received:2017-01-10 Revised:2017-02-27 Online:2017-03-31 Published:2017-03-31

摘要/Abstract

摘要：

目的：研究1,4-苯醌对人慢性髓系白血病细胞（K562细胞）线粒体功能及凋亡的影响。方法：分别用终浓度为0、10、20 μmol/L的1,4-苯醌处理K562细胞24 h，用CCK-8法检测细胞活力，通过流式细胞仪检测活性氧（ROS）生成量；用线粒体膜电位、三磷酸腺苷（ATP）生成量来评价线粒体功能；用PI-Annexin V双染法检测细胞的凋亡，采用分光光度法检测caspase-3酶的活性。结果：与对照组比较，1,4-苯醌10和20 μmol/L染毒组K562细胞相对增殖率均降低（P均<0.05）；随着1,4-苯醌浓度的增加，ROS生成量逐渐上升、线粒体膜电位和ATP生成量均逐渐降低、细胞的凋亡率逐渐增高，其中1,4-苯醌20 μmol/L染毒组与对照组间的差异均有统计学意义（P < 0.05或P < 0.01）；caspase-3活性逐渐升高，1,4-苯醌10和20 μmol/L染毒组与对照组相比差异均有统计学意义（P均<0.01）。结论：1,4-苯醌可以诱导K562细胞ROS升高，抑制K562细胞增殖，造成线粒体功能障碍，诱导细胞凋亡升高，提示线粒体障碍在1,4-苯醌诱导K562细胞凋亡的过程中发挥了重要作用。

关键词: 1,4-苯醌, K562细胞系, 细胞凋亡, 线粒体功能

Abstract:

OBJECTIVE: To determine effects of 1,4-BQ on mitochondrial dysfunction and apoptosis in human chronic myeloid leukemia cells (K562 cells). METHODS: K562 cells were treated with 0,10,and 20 μmol/L 1,4-BQ for 24 h. Cell viability was detected by CCK-8 assay,production of reactive oxygen species (ROS) was detected by flow cytometry;function of mitochondria was evaluated by measuring mitochondrial membrane potential and adenosine triphosphate (ATP);and caspase-3 enzyme activity was detected using spectrophotometry. RESULTS: Compared with the control,the relative growth rate of K562 cells in the 1,4-BQ 10 and 20 μmol/L treatment groups decreased with the increased concentration of 1,4-BQ (P < 0.05). Production of ROS and cell apoptosis rates were elevated while mitochondrial membrane potential and the amounts of ATP were reduced. Between the 1,4-BQ 20 μmol/L exposure groups and the control group,the difference was statistically significant (P < 0.05 or P < 0.01). The activity of caspase-3 was increased,and the difference was statistically significant (P < 0.01) between the control and both 1,4-BQ treatment groups. CONCLUSION: 1,4-BQ induced increase of ROS in K562 cells,inhibited their proliferation and resulted in mitochondrial dysfunction and expression of apoptosis. This indicates that mitochondrial dysfunction was involved with 1,4-BQ -induction of apoptosis in K562 cells.

Key words: 1,4-benzoquinone, K562 cell line, apoptosis, mitochondrial function

中图分类号:

R994.6

蒋小云, 孙蓉丽, 满招娣, 张娟, 浦跃朴. 1,4-苯醌致K562细胞线粒体功能障碍与凋亡作用[J]. 癌变·畸变·突变, 2017, 29(2): 129-133.

JIANG Xiaoyun, SUN Rongli, MAN Zhaodi, ZHANG Juan, PU Yuepu. Induction of mitochondrial dysfunction and apoptosis by 1,4-benzoquinone in K562 cells[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2017, 29(2): 129-133.

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1,4-苯醌致K562细胞线粒体功能障碍与凋亡作用

Induction of mitochondrial dysfunction and apoptosis by 1,4-benzoquinone in K562 cells

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