期刊文献+

Nrf2-ARE信号通路在神经系统疾病中的作用 被引量:4

原文传递
导出
摘要 多种因素可诱导机体产生氧化应激反应,包括外源性物质入侵、重金属及电离辐射、感染以及缺血-再灌注损伤等。氧化应激产生活性氧族(reactive oxygen species,ROS)及亲电子物质,其在体内堆积诱导产生氧化应激或亲电子应激,损伤细胞膜,致DNA加合物的形成及诱导突变,从而介导一系列病理变化乃至疾病发生。
作者 周圆圆 张泓
出处 《中华急诊医学杂志》 CAS CSCD 北大核心 2012年第4期444-446,共3页 Chinese Journal of Emergency Medicine
  • 相关文献

参考文献21

  • 1Satoh T,Okamoto S,Cui J. Activation of the keapl-Nrf2 pathway for neuroprotection by electrophillic phase Ⅱ inducers[J].Proceedings of the National Academy of Sciences(USA),2006,(03):768-773.
  • 2Yu X,Kensler T. Nrf2 as a target for cancer chemoprevention[J].Mutation Research,2005,(1/2):93-102.
  • 3Lee JM,Shih AY,Murphy TH,Johnson JA. NF-E2-related factor-2 mediateds neuroproteciton against mitochondrial complexⅠ inhibitors and increased concentrations of intracellular calcium in primary cortical neurons[J].Journal of Biological Chemistry,2003,(39):37948-37956.
  • 4Mizuno K,Kume T,Muto C. Glutathione biosynthesis via activation of the Nrf2-ARE pathway is essential for neuroprotective effects of sulforaphane and 6-(methylsulfinyl) hexyl isothiocyanate[J].Pharmacol Sci,2011,(03):320-328.doi:10.1254/jphs.10257FP.
  • 5Calkins M J,Jakel RJ,Johnson DA. Protection from mitochondrial complex Ⅱ inhibition in vitro and in vivo by Nrf2-mediated transcription[J].Proceedings of the National Academy of Sciences(USA),2005,(01):244-249.doi:10.1073/pnas.0408487101.
  • 6Kobayashi A,Kang MI,Okawa H. Oxidative stress sensor keapl functions as an adaptor for cu13-based E3 ligase to regulate proteasomal degradation of Nrf2[J].Molecular and Cellular Biology,2004,(16):7130-7139.doi:10.1128/MCB.24.16.7130-7139.2004.
  • 7Kobayash M,Yamamoto M. Nrf2-keapl regulation of cellular defense mechanisms against electrophiles and reactive oxygen species[J].Advances in Enzyme Regulation,2006.113-140.
  • 8Cullinan SB,Dichl A. PERK-dependent activation of Nrf2 conlributes to redox homeostasis and cell survival following endoplasmic reticulum stress[J].Journal of Biological Chemistry,2004,(19):20108-20117.doi:10.1074/jbc.M314219200.
  • 9Bloom DA,Jaiswal AK. Phosphorylation of Nrf2 at Ser40 by protcin kinase C in response to antioxidants leads to the release of Nrf2 from INrf2,but is not required for Nrf2 stabilization/accumulation in the nucleus and transcriptional activation of antioxidant response element-mediated NAD (P) H:quinine oxidoreductasc-1 gcne expression[J].Journal of Biological Chemistry,2003,(45):44675-44682.doi:10.1074/jbc.M307633200.
  • 10Sekhar KR,Rachakonda G,Michael L. Cysteine-based regulation of thecul3 adaptor protein keapl[J].Toxicol Appl,2010,(01):21-26.

同被引文献45

  • 1余剑波,姚尚龙,袁世荧,杨艳.血红素氧合酶-1对内毒素休克大鼠肺组织的保护功能[J].中华急诊医学杂志,2004,13(11):739-741. 被引量:6
  • 2李志军,刘红栓,王今达.血必净联合前列腺素E1防治急性肺纤维化的实验研究[J].中华急诊医学杂志,2007,16(3):255-259. 被引量:29
  • 3周长福,李志军,刘红栓.血必净联合前列腺素E_1对肺纤维化大鼠转化生长因子-β1的影响[J].中国中西医结合急救杂志,2007,14(3):186-186. 被引量:20
  • 4Constantin M, Choi AJ, Cloonan SM, et al. Therapeutic potential of heme oxygenase-1/carbon monoxide in lung disease [ J]. Int J Hypertens, 2012, 2012: 859235.
  • 5Murphey ED. CLP-induced impairment of innate immune function is caused by exposure to the cecal lumenal contents and not the tissue trauma or tissue ischemia/necrosis components [ J ]. Microbes Infect, 2012, 14 (1): 35-42.
  • 6Luo YP, Jiang L, Kang K, et al. Hemin inhibits NLRP3 inflammasome activation in sepsis-induced acute lung injury, involving heine oxygenase-1 [ J]. Int Immunopharmacol, 2014, 20 (1) : 24-32.
  • 7Marier JF, Chen K, Prince P, et al. Production of ex vivo lipopolysaceharide-induced tumor necrosis factor-alpha, interleukin- l beta, and interleukin-6 is suppressed by trans-resveratrol in a concentration-dependent manner [ J ]. Can J Vet Res, 2005, 69 (2) : 151-154.
  • 8Riedemann NC, Neff TA, Guo RF, et al. Protective effects of IL-6 blockade in sepsis are linked to reduced C5a receptor expression [J]. J Immunol, 2003, 170 (1) : 503-507.
  • 9Ryter SW, Otterbein LE, Morse D, et al. Heme oxygenasel carbon monoxide signaling pathways: regulation and functional significance [J]. Mol Cell Biochem, 2002, 234-235 (1/2) : 249-263.
  • 10Tsoyi K, Lee TY, Lee YS, et al. Heme-oxygenase-1 induction and carbon monoxide-releasing molecule inhibit lipopolysaccharide (LPS) -induced high-mobility group box 1 release in vitro and improve survival of mice in LPS- and cecM ligation and puncture- induced sepsis model in vivo [ J ]. Mol Pharmacol, 2009, 76 ( 1 ) : 173-182.

引证文献4

二级引证文献14

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