期刊文献+

丙泊酚对小胶质细胞焦亡的影响及其潜在机制 被引量:1

Effect and potential mechanism of propofol on microglial pyroptosis
下载PDF
导出
摘要 目的探讨丙泊酚对小胶质细胞焦亡的影响及其潜在机制。方法250μmol/L丙泊酚处理小鼠小胶质BV2细胞3 h,检测线粒体膜电位、线粒体活性氧、线粒体呼吸链复合物Ⅰ酶活性及NLRP3、ASC、caspase-1、GSDMD、IL 1β、LC3B、p62、COX4I1、cathepsin B表达。结果丙泊酚引起BV2细胞线粒体损伤、NLRP3炎症小体介导的焦亡,并抑制线粒体自噬。结论丙泊酚可通过抑制线粒体功能介导BV2细胞焦亡。 Objective To study the effect of and potential mechanism of propofol on microglial pyroptosis.Methods After treated with 250μmol/L propofol for 3 h,mitochondrial membrane potential,reactive oxygen species,respiratory chain complex I enzyme activity,and expression of NLRP3,ASC,caspase-1,GSDMD,IL-1β,LC3B,p62,COX4I1,and cathepsin B were determined in mouse microglia BV2.Results Propofol induced mitochondrial damage and NLRP3 inflammasome mediated pyroptosis,and suppressed mitophagy in BV2 cells.Conclusion Propofol can mediate pyroptosis of BV2 cells via inhibiting mitochondrial function.
作者 戴中亮 田迪 张洪研 高文莉 林苗 宋意锋 田雅 邢燕梅 DAI Zhong-liang;TIAN Di;ZHANG Hong-yan;GAO Wen-li;LIN Miao;SONG Yi-feng;TIAN Ya;XING Yan-mei(Department of Anesthesiology,Second Clinical Medical College of Jinan University,First Affiliated Hospital of Southern University of Science and Technology,Shenzhen People􀆳s Hospita,Shenzhen 518020,China)
出处 《广东医科大学学报》 2021年第5期534-538,共5页 Journal of Guangdong Medical University
基金 国家自然科学基金(No.81703263) 广东省医学科研基金(No.A2019382) 深圳市卫计委科研基金(No.SZXJ2017029)。
关键词 丙泊酚 线粒体损伤 线粒体自噬 焦亡 propofol mitochondrial damage mitophagy pyroptosis
  • 相关文献

参考文献4

二级参考文献39

  • 1Hildeman DA,Mitchell T,Kappler J,et al.Tcell apopto-sis and reactive oxygen species[].The Journal of Clinical Investigation.2003
  • 2Villamor N,Montserrat E,Colomer D.Cytotoxic effects of Blymphocytes mediated by reactive oxygen species[].Current Pharmaceutical Design.2004
  • 3Jackson SH,Devadas S,Kwon J,et al.T cells express a phagocyte-type NADPHoxidase that is activated after Tcell receptor sti mulation[].Nature Immunology.2004
  • 4Tse HM,Milton MJ,Piganelli JD.Mechanistic analysis of the i mmunomodulatory effects of a catalytic antioxidant on antigen-presenting cells:i mplication for their use intarge-ting oxidation-reduction reactions in innate i mmunity[].Free Radical Biology and Medicine.2004
  • 5Thoren FB,Betten A,Romero AI,et al.Cutting edge:antioxidative properties of myeloid dendritic cells:protection of Tcells and NKcells fromoxygen radical-inducedinactiva-tion and apoptosis[].J I mmunol.2007
  • 6Tse HM,Milton MJ,Schreiner S,et al.Disruption of in-nate-mediated proinflammatory cytokine and reactive oxygen species third signal leads to antigen-specific hyporesponsive-ness[].J I mmunol.2007
  • 7Jones RG,Bui T,White C,et al.The proapoptotic factors Bax and Bak regulate T cell proliferation through control of endoplasmic reticulum Ca2+homeostasis[].I mmunity.2007
  • 8Gloire G,Legrand-Poels S,Piette J.NF-kappaB activation by reactive oxygen species:fifteen years later[].Biochemical Pharmacology.2006
  • 9Gloire G,Charlier E,Rahmouni S,et al.Restoration of SHIP-1activity in human leukemic cells modifies NF-kappaB activation pathway and cellular survival upon oxidative stress[].Oncegene.2006
  • 10Murata Y,Ohteki T,Koyasu S,et al.IFN-gamma and pro-inflammatory cytokine production by antigen-presenting cells is dictated byintracellular thiol redox status regulated by oxygen tension[].European Journal of Immunology.2002

共引文献454

同被引文献17

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部