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光甘草定诱导小鼠黑色素瘤B16F10细胞凋亡的机制研究

高彩霞 王艳明 李德芳 唐晓峰 郑秋生

天然产物研究与开发2017,Vol.29Issue(5):836-842,7.
天然产物研究与开发2017,Vol.29Issue(5):836-842,7.DOI:10.16333/j.1001-6880.2017.5.021

光甘草定诱导小鼠黑色素瘤B16F10细胞凋亡的机制研究

Glabridin Induces Apoptosis in Melanoma B16F10 Cells by Altering Glycolysis

高彩霞 1王艳明 2李德芳 1唐晓峰 3郑秋生1

作者信息

  • 1. 滨州医学院中西医结合学院,烟台264003
  • 2. 博州人民医院药剂科,新疆833400
  • 3. 烟台大学生命科学学院,烟台264003
  • 折叠

摘要

Abstract

To explore the molecular mechanism of glabridin-induced B16F10 cell proliferation inhibition via in vitro and in vivo model of melanoma.Glabridin induced B16F10 cell proliferation inhibition and cell apoptosis in a dose-dependent manner.The Bax mRNA and protein expressions were up-regulated and the Bcl-2 was down-regulated in glabridin-treated B16F10 cells.Further studies showed that glabridin decreased the production of ATP and lactic acid in mouse melanoma B16F10 cells.Glabridin down-regulated the mRNA and protein expressions of glycolysis-related kinase genes (Hk2 and Ldha) in B16F10 cells.In addition,the animal model of mouse melanoma indicated that glabridin treatment suppressed tumor growth and induced tumor apoptosis.Both the mRNA and protein levels of glycoIysis-related kinase genes(Hk2 and Ldha) and Bcl-2 in tumor tissue were also decreased and Bax was increased in glabridin treated mice.It was concluded thatglabridin inhibited the proliferation and induced apoptosis of melanoma B16F10 cells in a dose-dependent manner,and the inhibition of glycolysis played a crucial role in the induction of apoptosis in glabridin-treated B16F10 cells.

关键词

光甘草定/B16F10细胞/糖酵解/细胞凋亡

Key words

glabridin/B16F10 cells/glycolysis/apoptosis

分类

医药卫生

引用本文复制引用

高彩霞,王艳明,李德芳,唐晓峰,郑秋生..光甘草定诱导小鼠黑色素瘤B16F10细胞凋亡的机制研究[J].天然产物研究与开发,2017,29(5):836-842,7.

基金项目

滨州医学院科研启动基金(BY2014KYQD01) (BY2014KYQD01)

国家自然科学基金(31471338) (31471338)

山东省高等学校优势学科人才团队培育计划 ()

天然产物研究与开发

OA北大核心CSCDCSTPCD

1001-6880

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