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Cell Mol Neurobiol. 2013 Mar;33(2):205-12. doi: 10.1007/s10571-012-9886-3. Epub 2012 Nov 15.

本文引用的文献

1
α-synuclein reactive antibodies as diagnostic biomarkers in blood sera of Parkinson's disease patients.α-突触核蛋白反应性抗体作为帕金森病患者血清中的诊断生物标志物。
PLoS One. 2011 Apr 25;6(4):e18513. doi: 10.1371/journal.pone.0018513.
2
Proteomic analysis of dopamine and α-synuclein interplay in a cellular model of Parkinson's disease pathogenesis.帕金森病发病机制细胞模型中多巴胺与α-突触核蛋白相互作用的蛋白质组学分析。
FEBS J. 2010 Dec;277(23):4909-19. doi: 10.1111/j.1742-4658.2010.07896.x. Epub 2010 Oct 26.
3
Identification of glutathione S-transferase pi as a protein involved in Parkinson disease progression.鉴定谷胱甘肽S-转移酶π为参与帕金森病进展的一种蛋白质。
Am J Pathol. 2009 Jul;175(1):54-65. doi: 10.2353/ajpath.2009.081019. Epub 2009 Jun 4.
4
Oxidative stress in Parkinson's disease: a mechanism of pathogenic and therapeutic significance.帕金森病中的氧化应激:一种具有致病和治疗意义的机制。
Ann N Y Acad Sci. 2008 Dec;1147:93-104. doi: 10.1196/annals.1427.023.
5
Proteome analysis of human substantia nigra in Parkinson's disease.帕金森病患者黑质的蛋白质组分析
Proteome Sci. 2008 Feb 14;6:8. doi: 10.1186/1477-5956-6-8.
6
Response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) differs in mouse strains and reveals a divergence in JNK signaling and COX-2 induction prior to loss of neurons in the substantia nigra pars compacta.对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)的反应在不同小鼠品系中存在差异,并且在黑质致密部神经元丧失之前,显示出JNK信号传导和COX-2诱导方面的差异。
Brain Res. 2007 Oct 17;1175:107-16. doi: 10.1016/j.brainres.2007.07.067. Epub 2007 Aug 9.
7
GSTpi expression mediates dopaminergic neuron sensitivity in experimental parkinsonism.谷胱甘肽S-转移酶π(GSTpi)的表达介导了实验性帕金森病中多巴胺能神经元的敏感性。
Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):1977-82. doi: 10.1073/pnas.0610978104. Epub 2007 Jan 31.
8
Glutathione S-transferase polymorphisms and onset age in alpha-synuclein A53T mutant Parkinson's disease.谷胱甘肽S-转移酶基因多态性与α-突触核蛋白A53T突变型帕金森病的发病年龄
Am J Med Genet B Neuropsychiatr Genet. 2007 Mar 5;144B(2):254-8. doi: 10.1002/ajmg.b.30450.
9
Increased glutathione S-transferase activity rescues dopaminergic neuron loss in a Drosophila model of Parkinson's disease.谷胱甘肽S-转移酶活性增加可挽救帕金森病果蝇模型中的多巴胺能神经元损失。
Proc Natl Acad Sci U S A. 2005 May 31;102(22):8024-9. doi: 10.1073/pnas.0501078102. Epub 2005 May 23.
10
Glutathione transferases.谷胱甘肽转移酶
Annu Rev Pharmacol Toxicol. 2005;45:51-88. doi: 10.1146/annurev.pharmtox.45.120403.095857.

帕金森病患者血液中 MPP+ 诱导的氧化应激后谷胱甘肽 S-转移酶 pi 表达的改变。

Alterations in glutathione S-transferase pi expression following exposure to MPP+ -induced oxidative stress in the blood of Parkinson's disease patients.

机构信息

Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.

出版信息

Parkinsonism Relat Disord. 2011 Dec;17(10):765-8. doi: 10.1016/j.parkreldis.2011.06.026. Epub 2011 Aug 12.

DOI:10.1016/j.parkreldis.2011.06.026
PMID:21840241
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3307132/
Abstract

The major motor symptoms of Parkinson's disease do not occur until a majority of the dopaminergic neurons in the midbrain SNpc have already died. For this reason, it is critical to identify biomarkers that will allow for the identification of presymptomatic individuals. In this study, we examine the baseline expression of the anti-oxidant protein glutathione S-transferase pi (GSTpi) in the blood of PD patients and environmentally- and age-matched controls and compare it to GSTpi levels following exposure to 1-methyl-4-phenylpyridinium (MPP(+)), an agent that has been shown to induce oxidative stress. We find that after 4 h of exposure to MPP(+), significant increases in GSTpi levels can be observed in the leukocytes of PD patients. No changes were seen in other blood components. This suggests that GSTpi and potentially other members of this and other anti-oxidant families may be viable biomarkers for PD.

摘要

帕金森病的主要运动症状直到中脑 SNpc 中的多巴胺能神经元已经大量死亡才会出现。出于这个原因,识别能够识别出无症状个体的生物标志物至关重要。在这项研究中,我们检查了帕金森病患者和环境及年龄匹配对照者血液中抗氧化蛋白谷胱甘肽 S-转移酶 pi (GSTpi) 的基线表达水平,并将其与暴露于 1-甲基-4-苯基吡啶鎓 (MPP(+)) 后的 GSTpi 水平进行了比较,MPP(+) 是一种已被证明会引起氧化应激的物质。我们发现,在暴露于 MPP(+) 4 小时后,帕金森病患者的白细胞中 GSTpi 水平会显著升高。其他血液成分没有变化。这表明 GSTpi 以及可能的其他抗氧化家族成员可能是帕金森病的可行生物标志物。