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抗霉素A诱导血小板凋亡的分子机制研究

胡萍 朱永明 谢如锋 王志成

安徽医科大学学报Issue(11):1588-1592,1593,6.
安徽医科大学学报Issue(11):1588-1592,1593,6.

抗霉素A诱导血小板凋亡的分子机制研究

Study of molecular mechanisms on platelet apoptosis induced by antimycin A

胡萍 1朱永明 1谢如锋 2王志成3

作者信息

  • 1. 华东师范大学生命科学学院,上海 200062
  • 2. 上海市血液中心血液工程研究室,上海 200051
  • 3. 上海市血液中心血液工程研究室,上海 200051
  • 折叠

摘要

Abstract

Objective To investigate the effects and molecular mechanism of platelet apoptosis induced by Antimy-cin A (AMA).Methods Washed healthy volunteers platelets were pre-incubated with different concentration AMA,and then depolarization of mitochondrial membrane potential (ΔΨm),phosphatidylserine (PS)externaliza-tion assay,the surface expression of P-selectin,the activation of integrin αIIβ3 and the production of intracellular reactive oxygen species (ROS),mitochondrial ROS were detected by flow cytometry.The activation of Caspase-3 was analyzed by Western blot.In inhibition experiment,washed platelets were pre-incubated mitochondrial ROS targeted antagonists Mito-TEMPO,and then stimulated with different concentration AMA.The apoptosis associated indicators were detected by flow cytometry.Results AMA dose-dependently induces depolarization of ΔΨm,PS exposure,Caspase-3 activation,and the production of intracellular ROS and mitochondrial ROS,but AMA does not induce platelet activation.Mito-TEMPO effectively reduces the depolarization of ΔΨm,PS exposure and the pro-duction of mitochondrial ROS which induced by the AMA.Conclusion AMA can induce platelet apoptosis,and mitochondria ROS may play an important role in the platelets apoptosis induced by the AMA.

关键词

血小板/凋亡/抗霉素A/线粒体/活性氧

Key words

platelets/apoptosis/antimycin A/mitochondria/reactive oxygen species

分类

医药卫生

引用本文复制引用

胡萍,朱永明,谢如锋,王志成..抗霉素A诱导血小板凋亡的分子机制研究[J].安徽医科大学学报,2015,(11):1588-1592,1593,6.

基金项目

国家自然科学基金(编号81270650);上海市自然科学基金资助项目 ()

安徽医科大学学报

OA北大核心CSTPCD

1000-1492

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