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秦皮乙素抑制多柔比星毒性的分子机制研究

李潇 徐繁 房亮 张圣林 姜海军 赵博

新医学2018,Vol.49Issue(5):322-325,4.
新医学2018,Vol.49Issue(5):322-325,4.DOI:10.3969/j.issn.0253-9802.2018.05.005

秦皮乙素抑制多柔比星毒性的分子机制研究

Molecular mechanism of the effect of esculetin on relieving doxorubicin toxicity

李潇 1徐繁 1房亮 1张圣林 1姜海军 1赵博1

作者信息

  • 1. 067000承德,承德医学院附属医院
  • 折叠

摘要

Abstract

Objective To investigate the protective effect and mechanism of esculetin(Esc)on doxorubicin(DOX)-induced injury in H9C2 cells. Methods H9C2 myocardiac cells were cultured and di-vided into the control,DOX and Esc+DOX groups. The ultrastructure of the cells in each group was observed by transmission electron microscope. The expression of Bmi-1 in each group was detected by western blot. The cells were then divided into three groups:DOX,Esc +DOX +NC siRNA and Esc +DOX +Bmi-1 siRNA groups. Western blot was used to detect the expression of Bmi-1 in each group. The cellular apoptosis and the content of intracellular reactive oxygen species(ROS)were detected by flow cytometry. Results In the DOX group,cell swelling and mitochondrial cristae breakeage were observed and the expression of Bmi-1 was signifi-cantly lower than that in the Esc +DOX group(P<0.01). In the Esc +DOX +Bmi-1 siRNA group,the quantity of apoptotic cells and the content of ROS were significantly higher than that in the Esc +DOX+NC siRNA group(both P<0.01),and the expression of Bmi-1 was significantly lower than that in the Esc+DOX+NC siRNA group(P<0.01). Conclusions Esc can mitigate the DOX-induced injury in the H9C2 cells. The underlying mechanism is probably correlated with the down-regulated expression level of Bmi-1,thereby modulating the mitochondrial function and reducing the production of ROS.

关键词

多柔比星/秦皮乙素/线粒体/Bmi-1

Key words

Doxorubicin/Esculetin/Mitochondria/Bmi-1

引用本文复制引用

李潇,徐繁,房亮,张圣林,姜海军,赵博..秦皮乙素抑制多柔比星毒性的分子机制研究[J].新医学,2018,49(5):322-325,4.

基金项目

河北省医学科学研究重点课题计划(20170886) (20170886)

新医学

OACSTPCD

0253-9802

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