三氧化二砷通过 JNK 信号通路诱导 K562 细胞凋亡

中国临床药理学与治疗学 ›› 2008, Vol. 13 ›› Issue (10): 1099-1103.

三氧化二砷通过 JNK 信号通路诱导 K562 细胞凋亡

章圣辉, 韩义香, 吴建波, 叶爱芳, 尹丽慧, 谭映霞

温州医学院附属第一医院医学科学研究所, 温州 325000, 浙江

收稿日期:2008-08-02 修回日期:2008-09-15 出版日期:2008-10-26 发布日期:2020-10-19
作者简介:章圣辉, 男, 硕士, 主管技师, 研究方向:免疫学及细胞生物学。Tel:0577-86550276 　E-mail:shenghuizhang1@126.com

Apoptosis in K562 cells induced by arsenic trioxide via JNK signaling pathway

ZHANG Sheng-hui, HAN Yi-xiang, WU Jian-bo, YE Ai-fang, YIN Li-hui, TAN Ying-xia

Institute of Medical Science, the First Affiliated Hospital of Wenzhou Medical College, Wenzhou325000, Zhejiang,China

Received:2008-08-02 Revised:2008-09-15 Online:2008-10-26 Published:2020-10-19

摘要/Abstract

摘要： 目的: 探讨c-Jun氨基末端激酶(JNK)信号通路在三氧化二砷(As₂O₃)诱导K562细胞凋亡中的作用及机制。方法: 体外培养K562细胞,用As₂O₃ 及特异性JNK抑制剂SP600125对K562细胞进行处理;倒置相差显微镜下观察细胞形态学变化;MTT法检测不同时间点细胞增殖抑制率;Annexin V PI 染色结合流式细胞术检测细胞凋亡率;ELISA检测p-JNK蛋白表达的变化;流式细胞术检测突变型P53表达。结果: ELISA显示4μmol/L As₂O₃ 作用48 h后 p-JNK 蛋白表达增强,经SP600125 预处理后, As₂O₃ 诱导的K562细胞p-JNK蛋白表达明显减弱(P<0.01) , As₂O₃ 诱导的细胞增殖抑制率和细胞凋亡率均下降,与As₂O₃ 单作用组相比突变型P53表达增加(P<0.05)。结论: JNK信号转导通路在As₂O₃ 诱导K562细胞凋亡过程中发挥重要作用,是 As₂O₃ 诱导K562 细胞凋亡的主要途径之一。

关键词: 三氧化二砷, 人慢粒细胞系, K562, 细胞凋亡, p-JNK

Abstract: AIM: To investigate the role of c-jun N-terminal kinase (JNK) signaling pathway in the ap-optosis of human chronic myelogenous leukemia cell line K562 induced by arsenic trioxide and the possible mechanisms.METHODS: K562 cells were pre-incu-bated with SP600125 for 3 h prior to exposure to ar-senic trioxide at 4 μmol/L and for different time .The cell morphological changes were observed by inverted phase contrast microscopy .The cell growth inhibitory rate was detected by MTT colorimetric assay .The ap-optosis rate was analyzed by Annexin V/PI fluorescence staining together with flow cytometry .Changes in ex-pression of phospho-JNK protein were examined by ELISA.The mutant P53 expression was assayed by flow cytometry.RESULTS: Arsenic trioxide could significantly inhibit the proliferation of K562 cells and induce their apoptosis.The results of ELISA showed that the protein expression of phospho-JNK was in-creased in K562 cells after stimulated by Arsenic triox-ide.SP600125 remarkablely decreased the protein ex-pression of phospho-JNK as well as the apoptosis rate and the cell growth inhibitory rate, but the mutant P53 expression increased in K562 cells induced by arsenic trioxide as compared with those treated with only ar-senic trioxide.CONCLUSION: JNK signaling path-way may play an important role in the apoptosis of K562 cells induced by arsenic trioxide.

Key words: arsenic trioxide, human chronic my-elogenous leukemia cell line, K562, apoptosis, c-jun terminal kinase

中图分类号:

R737.9

章圣辉, 韩义香, 吴建波, 叶爱芳, 尹丽慧, 谭映霞. 三氧化二砷通过 JNK 信号通路诱导 K562 细胞凋亡[J]. 中国临床药理学与治疗学, 2008, 13(10): 1099-1103.

ZHANG Sheng-hui, HAN Yi-xiang, WU Jian-bo, YE Ai-fang, YIN Li-hui, TAN Ying-xia. Apoptosis in K562 cells induced by arsenic trioxide via JNK signaling pathway[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2008, 13(10): 1099-1103.

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