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自噬抑制剂在内质网应激状态下对肝癌HepG2细胞和正常肝细胞L-02作用的差异

李文成 刘加涛 高爽 于瀚卿 吴圣 范璐璐 孙国平

安徽医科大学学报Issue(7):884-887,888,5.
安徽医科大学学报Issue(7):884-887,888,5.

自噬抑制剂在内质网应激状态下对肝癌HepG2细胞和正常肝细胞L-02作用的差异

The different function of autophagy inhibitors between HepG2 liver cancer cells and normal liver cells L-02 in the endoplasmic reticulum stress state

李文成 1刘加涛 1高爽 1于瀚卿 1吴圣 1范璐璐 1孙国平1

作者信息

  • 1. 安徽医科大学第一附属医院肿瘤科,合肥 230022
  • 折叠

摘要

Abstract

Objective To investigate the difference in function of autophagy inhibitors between HepG2 and L-02 cells in the state of endoplasmic reticulum stress. Methods The HepG2 cells and L-02 cells were routinely cul-tured in vitro and treated either with tunicamycin ( TM) or combination with the autophagy inhibitors 3-methylade- <br> nine (3-MA) or chloroquine ( CQ) . The cell viability was detected by MTT assay. Cell apoptosis was detected by flow cytometry. The change of autophagy-related protein LC3 was analysed by Western blot assay. Results MTT assay demonstrated that TM could time-dependently induce the death of HepG2 cells and L-02 cells, and the cell viability of HepG2 cells was significantly restrained when it was administrated in combination with 3-MA or CQ, the cell survival rates of 24 h were:3-MA+TM (60%) , CQ+TM (72%) , TM (86%) respectively, and the differ-ence was statistically significant ( P<0. 01 ) . However, it had no significant effect with L-02 cells because of its cell survival rates of 24 h were:83%, 84% and 83%. Flow cytometry apoptosis experiment found that: TM+3-MA, CQ+TM and TM group on HepG2 cell apoptosis rates were 15%, 11% and 7% respectively, and the differ-ence was statistically significant(P<0. 01). But for L-02 cell group, the apoptosis rates were 16%, 17%, 16%which had no obvious difference. According to the results of Western blot, TM could cause increased autophagy, and autophagy inhibitor CQ could lead to increased autophagy tide. Conclusion The cell viability of HepG2 cells, not the L-02 cells, can be significantly restrained by TM combined with different autolysosome inhibitor 3-MA or CQ. So the autophagy can protect the hepatocarcinoma cell line HepG2 under the state of endoplasmic reticulum stress, and it can’ t provide the same protection to L-02 cell line.

关键词

自噬抑制剂/内质网应激/肝癌/肝正常细胞

Key words

autophagy inhibitors/endoplasmic reticulum stress/liver neoplasms/liver cell

分类

医药卫生

引用本文复制引用

李文成,刘加涛,高爽,于瀚卿,吴圣,范璐璐,孙国平..自噬抑制剂在内质网应激状态下对肝癌HepG2细胞和正常肝细胞L-02作用的差异[J].安徽医科大学学报,2015,(7):884-887,888,5.

基金项目

国家自然科学基金(编号:81272739) (编号:81272739)

安徽省科技攻关项目(编号:12010402122) (编号:12010402122)

安徽医科大学学报

OA北大核心CSTPCD

1000-1492

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