期刊文献+

Nrf2转录因子在脓毒症中的研究进展 被引量:7

Progress on nuclear factor-E2 related factor 2 transcription factors in sepsis
原文传递
导出
摘要 脓毒症是严重创伤、大面积烧伤、感染和大手术等急危重患者的严重并发症,可诱发脓毒性休克和多器官功能障碍综合征(MODS),其发病率和病死率一直居高不下.核转录因子-E2相关因子2(Nrf2)是抗氧化应激反应的重要转录因子,它通过调节抗氧化反应元件(ARE)介导的抗氧化酶和Ⅱ相解毒酶的表达,在脓毒症治疗中起关键作用.本文通过对Nrf2在脓毒症中的变化、相关调控机制及逆转措施进行综述,旨在为发掘脓毒症的有效干预措施提供参考. Sepsis is a critical complication of severe trauma, large area burns, infection, and major surgery etc., which can induce septic shock and multiple organ dysfunction syndrome (MODS), and its incidence and mortality are always high. Nuclear factor-E2 related factor 2 (Nrf 2) is an important transcription factor of antioxidant stress response. It plays a key role in the treatment of sepsis by regulating the expression of antioxidant enzyme and phase Ⅱ detoxification enzyme mediated by antioxidant response element (ARE). In this article we review the changes, related regulation mechanism and reversing measures of Nrf 2 in sepsis, aiming to provide a reference for the effective intervention measures of sepsis.
作者 王星玉 陈涛 马晓媛 黄文娟 黄祺 刘宽 梁华平 Wang Xingyu;Chen Tao;Ma Xiaoyuan;Huang Wenjuan;Huang Qi;Liu Kuan;Liang Huaping(Department of Intensive Care Unit,the Affiliated Hospital of Zunyi Medical University,Zunyi 563003,Guizhou,Chin;State Key Laboratory of Trauma,Burns and Combined Injury,Research Institute of Surgery of the Third Affiliated Hospital,the Army Military Medical University,Chongqing 400042,China)
出处 《中华危重病急救医学》 CAS CSCD 北大核心 2018年第8期810-814,共5页 Chinese Critical Care Medicine
基金 国家自然科学基金(81671906)
关键词 核转录因子-E2相关因子2 脓毒症 氧化应激 Nuclear factor-E2-related factor 2 Sepsis Antioxidant stress
  • 相关文献

参考文献7

二级参考文献94

  • 1黄剑伟,龙小毛.肺移植供肺保护研究进展[J].实用器官移植电子杂志,2014,2(2):117-119. 被引量:13
  • 2光吉博則,谷仁烨.氧化应激的病理生理作用[J].日本医学介绍,2007,28(4):150-152. 被引量:20
  • 3Nguyen HB, Rivers EP, Abrahamian FM, et al. Severe sepsis and septic shock: review of the literature and emergeney dep- artmentman-agementguidelines[J]. Ann Emerg Med, 2006,48 (1) :28-54.
  • 4Crimi E, Sica V, Slutsky AS, et al. Role of oxidative stress in experimental sepsis and multisystem organ dysfunction [J]. Free Radical Res,2006,40(7) :665-672.
  • 5Kobsyashim M, Yamamoto M. Nrf2-Keapl regulation of cellular defense mechan isma against eletrophiles and re- active oxygen species [J]. Adv Enzyme Regul, 2006, 46 (1) :113-140.
  • 6Silliman CC, Curtis BR, Kopko PM, et al. Donor antibod- ies to HNA-3a implicated in TRALI reactions prime neu-trophils and cause PMN mediated damage to human pul- monary microvascular endothelial cells in a two-event in vitro model[J]. Blood,2007,109(4) :1752-1755.
  • 7Hubbard WJ, Choudhry M, Schwacha MG, et al. Cecal ligation and puncture[J]. Shock, 2005,24 ( 1 ) : 52-57.
  • 8Sakaguchi S, Furusawa S. Oxidative stress and septic shock: metabolic aspects of oxygen-derived free radicals generated in the liver during en-dotoxemia[J]. FEMS Immunol Med Mi- crobiol,2006,47(2) :167-177.
  • 9Ware LB. Pathophysiology of acute lung injury and the a- cute respiratory distress syndrome [J]. Seminars Respir Crit Care Med, 2006,27 (4) : 337-349.
  • 10Kaspar JW, Niture SK, Jaiswal AK. Nrf2 : INrf2 (Keapl) signaling in oxidative stress[J]. Free Radio Biol Med, 2009,47(9) : 1304-1309.

共引文献151

同被引文献54

引证文献7

二级引证文献17

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