吉林大学学报(医学版)

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维生素K3诱导氧化应激经ERK信号途径介导HeLa细胞发生自噬

于春艳1，刘希2，于春荣3，张钰4，苏静4，刘玉和1，李洪岩4   

  1. （1.北华大学基础医学院病理学教研室，吉林 吉林132013；2. 北华大学化学与生物学院实验中心，吉林 吉林132013； 3.北京昭衍新药研究中心有限公司毒理部， 北京  100176；4.吉林大学基础医学院病理生理学教研室，吉林 长春 130021）
  • 收稿日期:2013-03-25 出版日期:2014-03-28 发布日期:2014-03-28
  • 通讯作者: 李洪岩 E-mail:hongyan@jlu.edu.cn
  • 作者简介:于春艳(1975-),女,吉林省吉林市人，副教授，医学博士，主要从事肿瘤病理学方面的研究。
  • 基金资助:

    国家自然科学基金资助课题（81202552，81272876）；吉林省教育厅科研基金资助课题（吉教科合字2011第117号，吉教科合字2012第394号

    ）；吉林省科技厅自然科学基金资助课题（201215103）

Autophagy of HeLa cells mediated by oxidative stress induced by vitamin K3 through ERK signal  pathway

YU Chun-yan1,LIU Xi2,YU Chun-rong3,ZHANG Yu4,SU Jing4,LIU Yu-he1,LI Hong-yan4   

  1. (1.   Department of Pathology,College of Basic Medical Sciences,Beihua University,Jilin 132013,China;2. Experiment Center,College of Chemistry and Biology,Beihua University,Jilin 132013,China;3.Department of Toxicology，JOINN Laboratories，Beijing 100176,China;4. Department of Pathophysiology,School of Basic Medical Sciences,Jilin University,Changchun 130021,China)
  • Received:2013-03-25 Online:2014-03-28 Published:2014-03-28

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摘要：

的:利用维生素K3（VK3）复制HeLa细胞氧化应激模型，探讨细胞外信号调节激酶（ERK）途径在氧化应激诱导自噬过程中的作用。方法：将人宫颈癌

HeLa细胞随机分为对照组、VK3组（30  μmol•L-1）、U0126组（10  μmol•L-1）和VK3（30  μmol•L-1）+ U0126（10 μmol•L-1）组。MTT法检测

各组细胞生存率；Western blotting法检测HeLa细胞中ERK1/2、磷酸化ERK1/2（Phospho- ERK1/2）、自噬相关蛋白LC3-Ⅱ、凋亡相关蛋白caspase-3

及其活化片段cleaved caspase-3的表达水平；Hoechest 33342染色激光共聚焦观察凋亡细胞核形态和细胞凋亡率。结果：与VK3组比较，VK3+U0126组

HeLa细胞生存率降低（P<0.05）。VK3组作用2、4和8 h　HeLa细胞中Phospho-ERK1/2表达水平增加（P<0.05）。与对照组比较，VK3组HeLa细胞中LC3-

Ⅱ蛋白表达水平增加（P<0.05）；与VK3组比较，VK3+U0126组HeLa细胞中LC3-Ⅱ蛋白表达水平降低（P<0.05），cleaved caspase-3蛋白表达水平增加

（P<0.05）。与VK3组比较，VK3+U0126组HeLa细胞呈现凋亡细胞核形态，细胞凋亡率升高（P<0.05）。结论：氧化应激通过ERK信号途径诱导HeLa细胞

发生自噬，被激活的细胞自噬能抑制VK3诱导HeLa细胞凋亡。

关键词:  , 氧化应激；细胞外信号调节激酶；自噬；HeLa细胞

Abstract:

o establish oxidative stress model of HeLa cells copied by vitamin K3 (VK3),and to investigate the role of external signal-

regulated kinase (ERK) pathway in autophagy induced by oxidative stress in HeLa cells. Methods HeLa cells were divided into control

group,VK3 group (30  μmol•L-1)， U0126 group (10 μmol•L-1)，and VK3 (30  μmol•L-1)+ U0126 group (10  μmol•L-1).The survival

rate of HeLa cells in each group was measured by MTT assay;the expression levels of external signal-regulated kinase 1/2

(ERK1/2),phosphorylated ERK 1/2 (Phospho-ERK1/2),microtubule-associated protein light chain 3-Ⅱ (LC3-Ⅱ),and cysteine aspartic

acid specific protease-3 (caspase-3),and its activated fragment cleaved caspase-3 were determined by Western blotting method;the

morphological changes of nuclear and apoptotic rate of HeLa cells  in each group were detected by Hoechst staining.Results Compared

with VK3 group,the survival rate of HeLa cells in VK3+U0126 group was decreased (P<0.05).The expressions of Phospho-ERK1/2 in HeLa

cells were increased after treated with VK3 for 2,4,and 8 h (P<0.05).Compared with control group， the expression of LC3-Ⅱ protein

 in VK3 group was increased(P<0.05).Compared with VK3 group,the expression of LC3-Ⅱ in HeLa cells in  VK3+U0126  group was

decreased(P<0.05),and the expression of cleaved caspase-3 protein was increased (P<0.05).Compared with VK3 group,the morphological

changes of nuclear appeared and the  apoptotic  rate  of  HeLa cells in   VK3+U0126 group was increased(P<0.05).Conclusion

Oxidative stress activates autophagy of HeLa cells induced by ERK signal pathway,and  the autophagy can inhibit the apoptosis of

HeLa cells induced by VK3.

Key words: oxidative stress, external signal-regulated kinase, autophagy, HeLa cells

中图分类号: 

  • R363.2
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