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神经保护的中性粒细胞碱性磷酸酶机制

NAP mechanisms of neuroprotection.

作者信息

Gozes Illana, Steingart Ruth A, Spier Avron D

机构信息

Department of Clinical Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.

出版信息

J Mol Neurosci. 2004;24(1):67-72. doi: 10.1385/JMN:24:1:067.

DOI:10.1385/JMN:24:1:067
PMID:15314252
Abstract

An 8-amino-acid peptide, NAPVSIPQ (NAP), was identified as the smallest active element of activity-dependent neuroprotective protein that exhibits potent neuroprotective action. Potential signal transduction pathways include cGMP production and interference with inflammatory mechanisms, tumor necrosis factor-alpha, and MAC1-related changes. Because of its intrinsic structure, NAP might interact with extracellular proteins and also transverse membranes. NAP-associated protection against oxidative stress, glucose deprivation, and apoptotic mechanisms suggests interference with fundamental processes. This paper identifies p53, a key regulator of cellular apoptosis, as an intracellular target for NAP's activity.

摘要

一种由8个氨基酸组成的肽,即NAPVSIPQ(NAP),被确定为活性依赖神经保护蛋白的最小活性元件,该蛋白具有强大的神经保护作用。潜在的信号转导途径包括环磷酸鸟苷(cGMP)的产生以及对炎症机制、肿瘤坏死因子-α和与MAC1相关变化的干扰。由于其内在结构,NAP可能与细胞外蛋白质相互作用,也可能穿过细胞膜。NAP对氧化应激、葡萄糖剥夺和凋亡机制的相关保护作用表明其对基本过程存在干扰。本文确定细胞凋亡的关键调节因子p53是NAP活性的细胞内靶点。

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1
NAP mechanisms of neuroprotection.神经保护的中性粒细胞碱性磷酸酶机制
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Ferulic acid provides neuroprotection against oxidative stress-related apoptosis after cerebral ischemia/reperfusion injury by inhibiting ICAM-1 mRNA expression in rats.阿魏酸通过抑制大鼠脑缺血/再灌注损伤后细胞间黏附分子-1(ICAM-1)的mRNA表达,对氧化应激相关的细胞凋亡提供神经保护作用。
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NAP, a peptide derived from the activity-dependent neuroprotective protein, modulates macrophage function.中性粒细胞碱性磷酸酶(NAP)是一种源自活性依赖神经保护蛋白的肽,可调节巨噬细胞功能。
Ann N Y Acad Sci. 2006 Jul;1070:500-6. doi: 10.1196/annals.1317.069.
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引用本文的文献

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Front Endocrinol (Lausanne). 2022 Mar 23;13:867442. doi: 10.3389/fendo.2022.867442. eCollection 2022.
2
Activity-Dependent Neuroprotective Protein (ADNP)-Derived Peptide (NAP) Counteracts UV-B Radiation-Induced ROS Formation in Corneal Epithelium.活性依赖的神经保护蛋白(ADNP)衍生肽(NAP)可对抗紫外线B辐射诱导的角膜上皮细胞活性氧生成。
Antioxidants (Basel). 2022 Jan 7;11(1):128. doi: 10.3390/antiox11010128.
3
Nap Interferes with Hypoxia-Inducible Factors and VEGF Expression in Retina of Diabetic Rats.

本文引用的文献

1
The neuroprotective peptide NAP inhibits the aggregation of the beta-amyloid peptide.神经保护肽NAP可抑制β-淀粉样肽的聚集。
Peptides. 2003 Sep;24(9):1413-23. doi: 10.1016/j.peptides.2003.08.005.
2
Activity-dependent neuroprotective protein: a novel gene essential for brain formation.活性依赖的神经保护蛋白:一种对脑形成至关重要的新基因。
Brain Res Dev Brain Res. 2003 Aug 12;144(1):83-90. doi: 10.1016/s0165-3806(03)00162-7.
3
Multiple signaling events in amyloid beta-induced, oxidative stress-dependent neuronal apoptosis.
午睡干扰糖尿病大鼠视网膜中缺氧诱导因子和血管内皮生长因子的表达。
J Mol Neurosci. 2017 Feb;61(2):256-266. doi: 10.1007/s12031-016-0869-6. Epub 2016 Dec 1.
4
Therapeutic strategies for the treatment of tauopathies: Hopes and challenges.治疗tau 病的治疗策略:希望与挑战。
Alzheimers Dement. 2016 Oct;12(10):1051-1065. doi: 10.1016/j.jalz.2016.06.006.
5
Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress.神经退行性疾病中通过氮氧化应激导致的线粒体功能障碍与细胞死亡
Brain Res. 2016 Apr 15;1637:34-55. doi: 10.1016/j.brainres.2016.02.016. Epub 2016 Feb 13.
6
The transcriptional regulator ADNP links the BAF (SWI/SNF) complexes with autism.转录调节因子ADNP将BAF(SWI/SNF)复合物与自闭症联系起来。
Am J Med Genet C Semin Med Genet. 2014 Sep;166C(3):315-26. doi: 10.1002/ajmg.c.31413. Epub 2014 Aug 28.
7
NAP reduces murine microvascular endothelial cells proliferation induced by hyperglycemia.NAP可降低高血糖诱导的小鼠微血管内皮细胞增殖。
J Mol Neurosci. 2014 Nov;54(3):405-13. doi: 10.1007/s12031-014-0335-2. Epub 2014 May 30.
8
Davunetide (NAP) protects the retina against early diabetic injury by reducing apoptotic death.达武奈肽(NAP)通过减少凋亡性死亡来保护视网膜免受早期糖尿病损伤。
J Mol Neurosci. 2014 Nov;54(3):395-404. doi: 10.1007/s12031-014-0244-4. Epub 2014 Feb 2.
9
Autophagy has a key role in the pathophysiology of schizophrenia.自噬在精神分裂症的病理生理学中起关键作用。
Mol Psychiatry. 2015 Feb;20(1):126-32. doi: 10.1038/mp.2013.174. Epub 2013 Dec 24.
10
NAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy.NAP(达文西肽)可挽救神经退行性变疾病果蝇模型中的神经元功能障碍。
Mol Psychiatry. 2013 Jul;18(7):834-42. doi: 10.1038/mp.2013.32. Epub 2013 Apr 16.
淀粉样β蛋白诱导的、氧化应激依赖性神经元凋亡中的多种信号事件。
Free Radic Biol Med. 2003 Jul 1;35(1):45-58. doi: 10.1016/s0891-5849(03)00244-2.
4
Differential effects of ethanol antagonism and neuroprotection in peptide fragment NAPVSIPQ prevention of ethanol-induced developmental toxicity.乙醇拮抗作用和神经保护在肽片段NAPVSIPQ预防乙醇诱导的发育毒性中的差异效应。
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8543-8. doi: 10.1073/pnas.1331636100. Epub 2003 Jun 13.
5
Injections of the neuroprotective peptide NAP to newborn mice attenuate head-injury-related dysfunction in adults.给新生小鼠注射神经保护肽NAP可减轻成年小鼠与头部损伤相关的功能障碍。
Neuroreport. 2003 Mar 3;14(3):481-4. doi: 10.1097/00001756-200303030-00037.
6
Abeta[25-35] peptide and iron promote apoptosis in lymphocytes by an oxidative stress mechanism: involvement of H2O2, caspase-3, NF-kappaB, p53 and c-Jun.β淀粉样蛋白[25-35]肽与铁通过氧化应激机制促进淋巴细胞凋亡:过氧化氢、半胱天冬酶-3、核因子κB、p53和c-Jun的参与
Neurotoxicology. 2002 Sep;23(3):351-65. doi: 10.1016/s0161-813x(02)00081-5.
7
NAP accelerates the performance of normal rats in the water maze.中性粒细胞碱性磷酸酶(NAP)可加快正常大鼠在水迷宫中的表现。
J Mol Neurosci. 2002 Aug-Oct;19(1-2):167-70. doi: 10.1007/s12031-002-0028-0.
8
NAP, a femtomolar-acting peptide, protects the brain against ischemic injury by reducing apoptotic death.NAP是一种具有飞摩尔作用的肽,通过减少凋亡性死亡来保护大脑免受缺血性损伤。
Stroke. 2002 Apr;33(4):1085-92. doi: 10.1161/01.str.0000014207.05597.d7.
9
A single administration of the peptide NAP induces long-term protective changes against the consequences of head injury: gene Atlas array analysis.单次给予肽 NAP 可诱导针对头部损伤后果的长期保护性变化:基因图谱阵列分析。
J Mol Neurosci. 2002 Feb-Apr;18(1-2):37-45. doi: 10.1385/JMN:18:1-2:37.
10
Vasoactive intestinal peptide and related molecules induce nitrite accumulation in the extracellular milieu of rat cerebral cortical cultures.血管活性肠肽及相关分子可诱导大鼠大脑皮质培养物细胞外环境中亚硝酸盐积累。
Neurosci Lett. 2001 Jul 20;307(3):167-70. doi: 10.1016/s0304-3940(01)01954-1.