医学临床研究
  2025年7月10日 星期四           首 页    |    期刊简介    |    编委会    |    投稿指南    |    期刊订阅    |    广告合作    |    留言板    |    联系我们    |    English
医学临床研究  2021, Vol. 38 Issue (4): 488-492    DOI: 10.3969/j.issn.1671-7171.2021.04.003
  论著 本期目录 | 过刊浏览 | 高级检索 |
大气细颗粒物PM2.5对人微血管内皮细胞坏死性凋亡的影响*
黄一丹1, 马丽1, 周祎琦1, 董良2, 黄春波3**
1.广西壮族自治区柳州市人民医院麻醉科,广西 柳州 545006;
2.遵义医科大学附属医院麻醉科,贵州 遵义 563000;
3.湖南怀化市麻阳苗族自治县人民医院神经外科,湖南 麻阳 419400
Effects of Atmospheric Fine Particulate Matter PM2.5 on Necroptosis of Human Microvascular Endothelial Cells
HUANG Yi-dan, MA Li, ZHOU Yi-qi, et al
Department of Anesthesiology, Liuzhou Municipal People's Hospital, Liuzhou Guangxi 545006
全文: PDF (1873 KB)   HTML (1 KB) 
输出: BibTeX | EndNote (RIS)      
摘要 【目的】 观察大气细颗粒物PM2.5对体外培养血管内皮细胞坏死性凋亡的影响。【方法】 以人微血管内皮细胞株(HMEC-1)为研究对象,应用系列浓度PM2.5处理24 h后,CCK-8检测HMEC-1细胞活力,试剂盒法检测培养上清液乳酸脱氢酶(LDH)的活性,Western blot法检测坏死性凋亡相关蛋白RIPK3和MLKL的表达及磷酸化水平,Transwell法检测HMEC-1细胞通透性改变。采用坏死性凋亡抑制剂(Necrostatin-1)处理后,观察PM2.5对HMEC-1坏死性凋亡、细胞损伤和通透性的影响。【结果】 PM2.5可呈剂量依赖性抑制HMEC-1的增殖,并增加培养上清液中LDH活性、RIPK3和MLKL的蛋白表达以及其磷酸化水平。Transwell检测结果表明PM2.5可增加单层血管内皮细胞通透性,而坏死性凋亡抑制剂Necrostatin-1预处理可显著性抑制PM2.5应激下血管内皮细胞RIPK3和MLKL的蛋白表达及磷酸化水平,降低上清液LDH活性和单层血管内皮细胞通透性。【结论】 PM2.5可诱导HMEC-1坏死性凋亡,损伤血管内皮完整性。
服务
把本文推荐给朋友
加入我的书架
加入引用管理器
E-mail Alert
RSS
作者相关文章
关键词 颗粒物内皮,血管/细胞学内皮细胞/代谢体外培养技术细胞凋亡    
Abstract【Objective】 To investigate the effect of atmospheric fine particles (particulate matter) PM2.5 on necroptosis of human vascular endothelial cells.【Methods】 After 24 hours of treatment with a series of concentrations of PM2.5, CCK-8 was used to detect cell viability in HMEC-1 cells (human microvascular endothelial cell line); and the culture supernatant was used to detect the level of lactate dehydrogenase (LDH) produced by HMEC-1 cells. Western blot method was applied to detect the expression and phosphorylation level of necroptosis-related proteins RIPK3 and MLKL. The permeability changes of vascular endothelial cells were measured by trans-well method. After treatment with necrostatin-1, an inhibitor of necroptosis, the effects of PM2.5 on necroptosis, cell damage and permeability of vascular endothelial cells were observed and evaulated. 【Results】 PM2.5 inhibited the proliferation of human microvascular endothelial cells in a dose-dependent manner. It increased the LDH activity in the culture supernatant and upregulated protein expression and phosphorylation levels of RIPK3 and MLKL. The result of trans-well assay showed that PM2.5 increased the permeability of monolayer vascular endothelial cells. The pretreatment of necrostatin-1, an inhibitor of necroptosis, significantly inhibited the protein expression and phosphorylation levels of RIPK3 and MLKL in vascular endothelial cells under PM2.5 stimulation, and reduced the activity of LDH in the supernatant and the permeability of monolayer vascular endothelial cells.【Conclusion】 PM2.5 induces necroptosis of vascular endothelial cells and impairs the integrity of vascular endothelium.
Key wordsParticulate Matter    Endothelium, Vascular/CY    Endothelial Cells/ME    In Vitro Techniques    Apoptosis
收稿日期: 2021-03-18     
中图分类号:  R135.98  
基金资助:* 国家自然科学基金资助项目(编号:81760019)
通讯作者: ** E-mail: 731734181@qq.com   
引用本文:   
黄一丹, 马丽, 周祎琦, 董良, 黄春波. 大气细颗粒物PM2.5对人微血管内皮细胞坏死性凋亡的影响*[J]. 医学临床研究, 2021, 38(4): 488-492.
HUANG Yi-dan, MA Li, ZHOU Yi-qi, et al. Effects of Atmospheric Fine Particulate Matter PM2.5 on Necroptosis of Human Microvascular Endothelial Cells. JOURNAL OF CLINICAL RESEARCH, 2021, 38(4): 488-492.
链接本文:  
http://journal07.magtech.org.cn/yxlcyj/CN/10.3969/j.issn.1671-7171.2021.04.003     或     http://journal07.magtech.org.cn/yxlcyj/CN/Y2021/V38/I4/488
版权所有 © 2013 医学临床研究杂志社  湘ICP备13012052号-1
办公地址:湖南省长沙市芙蓉区新军路43号煤炭大院主办公楼6楼621、623、632、636室 邮编:410011 电话(传真):0731-84824007 E-mail:jcr_cs.hn@vip.163.com
技术支持:北京玛格泰克科技发展有限公司 技术支持:support@magtech.com.cn