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香蜂草苷诱导人肝癌细胞株HepG2凋亡及其作用机制

朱勋帅 林兴 黄权芳 林军

天然产物研究与开发2017,Vol.29Issue(4):579-583,5.
天然产物研究与开发2017,Vol.29Issue(4):579-583,5.DOI:10.16333/j.1001-6880.2017.4.008

香蜂草苷诱导人肝癌细胞株HepG2凋亡及其作用机制

Apoptosis-inducing Effect of Didymin on Human Hepatoma Cell Line HepG 2 and Its Action Mechanism

朱勋帅 1林兴 1黄权芳 2林军1

作者信息

  • 1. 广西医科大学药学院,南宁530021
  • 2. 广西中医药大学第一附属医院,南宁530023
  • 折叠

摘要

Abstract

To investigate the effect of didymin on apoptosis of human hepatocellular carcinoma HepG2 cells and its action mechanism.MTT assay was used to investigate the effect of didymin on proliferation of HepG2 cells.Flow cytometry assay was used to analyze apoptosis rate of HepG2 cells.The effects of didymin on caspase-3 and caspase-9 activities were detected using available kits.The protein expressions of Bcl-2,Bax,RKIP,ERK and p-ERK were detected by Western blot.The experimental resultsshowedthatdidymin can inhibit HepG2 proliferation and induce cell apoptosis,by activating caspase-3 and-9,regulating Bax andBcl-2 level.Moreover,our study indicated that didyminincreased RKIPexpression,resulting in the inactivation of ERK/MAPK signaling pathways.

关键词

香蜂草苷/HepG2细胞/凋亡/Raf激酶抑制剂/ERK/MAPK信号通路

Key words

didymin/HepG2 cells/apoptosis/RKIP/ERK/MAPK signaling pathway

分类

医药卫生

引用本文复制引用

朱勋帅,林兴,黄权芳,林军..香蜂草苷诱导人肝癌细胞株HepG2凋亡及其作用机制[J].天然产物研究与开发,2017,29(4):579-583,5.

基金项目

国家自然科学基金(81260505 ()

81473431) ()

广西自然科学基金(2014GXNSFAA118154) (2014GXNSFAA118154)

天然产物研究与开发

OA北大核心CSCDCSTPCD

1001-6880

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