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异丙酚对热打击后内皮细胞线粒体氧化应激损伤的保护作用

李莉 古正涛 何旋 邹志敏 潘志国 赵明 苏磊

解放军医学杂志2017,Vol.42Issue(6):500-505,6.
解放军医学杂志2017,Vol.42Issue(6):500-505,6.DOI:10.11855/j.issn.0577-7402.2017.06.04

异丙酚对热打击后内皮细胞线粒体氧化应激损伤的保护作用

Propofol alleviate oxidative stress and mitochondrial damage in endothelial cells after heat stress

李莉 1古正涛 1何旋 2邹志敏 2潘志国 3赵明 4苏磊3

作者信息

  • 1. 510630 广州 南方医科大学第三附属医院重症医学科
  • 2. 510515 广州 南方医科大学第一临床医学院
  • 3. 510010 广州 广州军区广州总医院重症医学科、全军热区创伤救治与组织修复重点实验室
  • 4. 510515 广州 南方医科大学基础医学院病理生理学教研室、广东省休克微循环重点实验室
  • 折叠

摘要

Abstract

Objective To explore the protective effect of propofol on endothelial cells during heat stress and its protective effect to mitochondra. Methods Heat stress model of human umbilical vein endothelial cell was established when cells were incubated at 43℃ for 2h, then further incubted at 37℃, 5%CO2 for 6h. The experimental group was subdivided into six groups, including 37℃ group, 37℃ plus intralipid group (negative control group), 37℃ plus propofol group, 43℃ plus propofol group, 43℃ plus intralipid group, H2O2 plus propofol group (positive control group); Pretreated with 50μmol/L propofol, 0.2ml intralipid or 25μmol/L H2O2 before heat stress at 43℃, while the cells in the control group were incubated at 37℃. Cell viability was tested by CCK-8. ROS, mitochondrial membrane potential and the changes in mitochondrial permeability transition pore were determined by flow cytometry. The level of ATP was detected by fluorescein-luciferase. The changes of caspase-9 and caspase-3 were analyzed by Caspase Activity Assay Kit. Results HUVESs cell viability and damage of mitochondra were significantly decreased after heat stress. Compared with 43℃ heat stress group, pretreatment with propofol induced the recovery of cell viability and the ROS levels were significantly decreased in HUVEC cells (P<0.05). Meanwhile, the number of cells representing the decrease of mitochondrial membrane potential (the proportion of JC-1 monomer) was significantly decreased (P<0.05) by propofol. The average fluorescence intensity of calcein which representing the MPTP changes and intracellular ATP content was significantly increased (P<0.05). In addition, the activation of mitochondrial apoptotic pathway mediated by caspase-9/3 was also inhibited. Conclusions Propofol have anti-oxidative, anti-apoptosis and mitochondria protective effect against endothelial cell injury during heat stress.

关键词

中暑/内皮细胞/氧化性应激

Key words

heat stroke/endothelial cells/oxidative stress

分类

医药卫生

引用本文复制引用

李莉,古正涛,何旋,邹志敏,潘志国,赵明,苏磊..异丙酚对热打击后内皮细胞线粒体氧化应激损伤的保护作用[J].解放军医学杂志,2017,42(6):500-505,6.

基金项目

广东省自然科学基金面上项目(2014A030313601) (2014A030313601)

广东省自然科学基金研究团队项目(S2013030013217) (S2013030013217)

广东省科技计划项目(2014A020212490,2013B031800010) (2014A020212490,2013B031800010)

南方医科大学校科研启动计划项目(PY2015NO29,QD2016N017)This work was supported by the Natural Science Foundation of Guangdong Province (2014A030313601) (PY2015NO29,QD2016N017)

Natural Science Foundation Research Team Project of Guangdong Province (S2013030013217) (S2013030013217)

Science and Technology Planning Project of Guangdong Province (2014A020212490, 2013B031800010) (2014A020212490, 2013B031800010)

the Scientific Research Starting Foundation for Southern Medical University (PY2015N029, QD2016N017) (PY2015N029, QD2016N017)

解放军医学杂志

OA北大核心CSCDCSTPCD

0577-7402

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