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硫化氢对氧化型低密度脂蛋白诱导的人脐静脉内皮细胞凋亡的影响

任重 赵战芝 彭湘萍 谢巍 刘艳文 索荣 姜志胜

中国动脉硬化杂志2011,Vol.19Issue(11):891-896,6.
中国动脉硬化杂志2011,Vol.19Issue(11):891-896,6.

硫化氢对氧化型低密度脂蛋白诱导的人脐静脉内皮细胞凋亡的影响

Investigation on the Effect and Mechanisms of Hydrogen Sulfide Against Apoptosis Induced bv ox-LDL in Human Umbilical Vein Endothelial Cells

任重 1赵战芝 2彭湘萍 1谢巍 2刘艳文 1索荣 2姜志胜1

作者信息

  • 1. 南华大学心血管疾病研究所
  • 2. 动脉硬化学湖南省重点实验室,湖南省衡阳市421001
  • 折叠

摘要

Abstract

Aim To investigate the effects of hydrogen sulfide on ox-LDL-induced apoptosis in human umbilical vein endothelial cells (HUVEC) and the mechanisms involved. Methods The HUVEC were incubated with ox-LDL for 24 hours after treatment with NaHS at different concentrations (25, 50, 100, 200 umol/L) for 24 hours or for different incubation time(6, 12, 24 hours) at the concentration of 50 ujnol/L. The apoptotic alterations of HUVEC were observed by Hoechst 33258 staining and flow cytometry (FCM) , respectively. The change of mitochondrial membrane potential (MMP) and intracellular reactive oxygen species(ROS) generation were detected by Dihydrohodaminel23 (DHR123) staining and rhodaminel23 (Rhl23) staining. Results Pre-treatment with NaHS remarkably inhibited apoptosis induced by ox-LDL in HUVEC in a time- and concentration-dependent manner( all P <0. 01). The decrease of MMP and increase of the intracellular ROS generation in HUVEC induced by ox-LDL were significantly prohibited by treatment with NaHS or N- acetyl-L-cysteine (NAC) (all P <0.05). Conclusions H2S inhibits apoptosis induced by ox-LDL in HUVEC which is involved in preservation of mitochondrial membrane potential and attenuation of the intracellular ROS generation.

关键词

硫化氢/氧化型低密度脂蛋白/N-乙酰半胱氨酸/人脐静脉内皮细胞/凋亡/细胞线粒体膜电位/细胞内活性氧

Key words

Hydrogen Sulfide/ ox-LDL/ NAC/ HUVEC/ Apoptosis/ Mitochondrial Membrane Potential/Reactive Oxygen Species

分类

医药卫生

引用本文复制引用

任重,赵战芝,彭湘萍,谢巍,刘艳文,索荣,姜志胜..硫化氢对氧化型低密度脂蛋白诱导的人脐静脉内皮细胞凋亡的影响[J].中国动脉硬化杂志,2011,19(11):891-896,6.

基金项目

国家自然科学基金项目(30971169)和衡阳市科学技术发展计划项目(2009KJ1O) (30971169)

中国动脉硬化杂志

OA北大核心CSCDCSTPCD

1007-3949

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