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大黄素诱导对内质网应激相关蛋白表达及肝癌HepG2细胞凋亡的影响

党中峰 党雅梅 陈城 蔡伟 郭应芳 杨华 那光伟 何科基

兰州大学学报(医学版)Issue(2):50-54,5.
兰州大学学报(医学版)Issue(2):50-54,5.DOI:10.13885/j.issn.1000-2812.2015.02.010

大黄素诱导对内质网应激相关蛋白表达及肝癌HepG2细胞凋亡的影响

Emodin induces endoplasmic reticulum stress-associated apoptosis in hepatocellular carcinoma HepG2 cell line

党中峰 1党雅梅 2陈城 2蔡伟 2郭应芳 2杨华 2那光伟 1何科基1

作者信息

  • 1. 甘肃省肿瘤医院 腹外二科,甘肃 兰州 730050
  • 2. 甘肃省人民医院 病理科,甘肃 兰州 730000
  • 折叠

摘要

Abstract

Objective To investigate the effect of emodin on the expression of endoplasmic reticulum stress (ERS)-associated proteins in hepatocellular carcinoma HepG2 cells. Methods After treatment with various concentrations of emodin(0, 10, 50, 100μmol/L), tumor cell viability and apoptosis were measured by MTT (methyl thiazolyl tetrazolium )and flow cytometry assays, respectively. The GRP78 (glucose-regulated pro-tein 78), CHOP(C/EBP homologous protein), caspase-12 were analysed by Western Blotting. Results Emodin inhibited the proliferation of HepG2 cells, promoted their apoptosis in the concentration-depandent manner and enhanced the expression of ERS chaperone GRP78 in HepG2 cells. Emodin treament also increased the expression of the two known essential ERS-associated apoptotic proteins, CHOP and caspase-12 and elevated caspase-12 activation in HepG2 cells. Conclusion Emodin induces apoptosis in hepatocellular carcinoma HepG2 cells probably involving the induction of ERS associated proteins.

关键词

大黄素/增殖/内质网应激/HepG2细胞

Key words

Emodin/proliferation/endoplasmic reticulum stress/HepG2 cells

分类

医药卫生

引用本文复制引用

党中峰,党雅梅,陈城,蔡伟,郭应芳,杨华,那光伟,何科基..大黄素诱导对内质网应激相关蛋白表达及肝癌HepG2细胞凋亡的影响[J].兰州大学学报(医学版),2015,(2):50-54,5.

基金项目

甘肃省中医药管理局科研项目 ()

兰州大学学报(医学版)

OACSTPCD

1000-2812

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