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德尔塔阿片受体及其肽:一种受体-配体神经保护。

Delta opioid receptor and its peptide: a receptor-ligand neuroprotection.

机构信息

Department of Neurosurgery and Brain Repair, University of South Florida College of Medicine, Tampa, FL 33612, USA.

出版信息

Int J Mol Sci. 2013 Aug 23;14(9):17410-9. doi: 10.3390/ijms140917410.

DOI:10.3390/ijms140917410
PMID:23979422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3794733/
Abstract

In pursuit of neurological therapies, the opioid system, specifically delta opioid receptors and delta opioid peptides, demonstrates promising therapeutic potential for stroke, Parkinson's disease, and other degenerative neurological conditions. Recent studies offer strong evidence in support of the therapeutic use of delta opioid receptors, and provide insights into the underlying mechanisms of action. Delta opioid receptors have been shown to confer protective effects by mediating ionic homeostasis and activating endogenous neuroprotective pathways. Additionally, delta opioid agonists such as (D-Ala 2, D-Leu 5) enkephalin (DADLE) have been shown to decrease apoptosis and promote neuronal survival. In its entirety, the delta opioid system represents a promising target for neural therapies.

摘要

为了寻求神经治疗方法,阿片系统,特别是δ阿片受体和 δ 阿片肽,在中风、帕金森病和其他神经退行性疾病方面显示出有希望的治疗潜力。最近的研究为 δ 阿片受体的治疗用途提供了强有力的证据,并深入了解其作用机制。δ 阿片受体通过调节离子动态平衡和激活内源性神经保护途径,发挥保护作用。此外,δ 阿片激动剂,如(D-Ala 2, D-Leu 5)脑啡肽(DADLE),已被证明可减少细胞凋亡并促进神经元存活。总的来说,δ 阿片系统是神经治疗的一个很有前途的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08b1/3794733/a87d970c0ff1/ijms-14-17410f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08b1/3794733/a87d970c0ff1/ijms-14-17410f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08b1/3794733/a87d970c0ff1/ijms-14-17410f1.jpg

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Int J Mol Sci. 2013 Aug 23;14(9):17410-9. doi: 10.3390/ijms140917410.
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Plant-Derived Antioxidants Protect the Nervous System From Aging by Inhibiting Oxidative Stress.植物源抗氧化剂通过抑制氧化应激保护神经系统免受衰老影响。
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本文引用的文献

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Current research on opioid receptor function.当前阿片受体功能的研究。
Curr Drug Targets. 2012 Feb;13(2):230-46. doi: 10.2174/138945012799201612.
2
Ionic storm in hypoxic/ischemic stress: can opioid receptors subside it?缺氧/缺血应激中的离子风暴:阿片受体能否抑制它?
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A novel insight into neuroprotection against hypoxic/ischemic stress.对缺氧/缺血应激神经保护的新见解。
Role of miR-326 in neonatal hypoxic-ischemic brain damage pathogenesis through targeting of the δ-opioid receptor.
miR-326 通过靶向 δ 阿片受体在新生儿缺氧缺血性脑损伤发病机制中的作用。
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Neuroprotective and neuroregenerative potential of pharmacologically-induced hypothermia with D-alanine D-leucine enkephalin in brain injury.D-丙氨酸-D-亮氨酸脑啡肽诱导的药物性低温对脑损伤的神经保护和神经再生潜力
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δ-Opioid Receptor Activation Attenuates the Oligomer Formation Induced by Hypoxia and/or α-Synuclein Overexpression/Mutation Through Dual Signaling Pathways.δ-阿片受体激活通过双重信号通路减轻缺氧和/或α-突触核蛋白过表达/突变诱导的寡聚体形成。
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A novel mechanism for cytoprotection against hypoxic injury: δ-opioid receptor-mediated increase in Nrf2 translocation.一种针对缺氧损伤的细胞保护新机制:δ-阿片受体介导的Nrf2易位增加。
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Sheng Li Xue Bao. 2009 Dec 25;61(6):585-92.
4
Delta opioid peptide DADLE and naltrexone cause cell cycle arrest and differentiation in a CNS neural progenitor cell line.德尔塔阿片肽 DADLE 和纳曲酮导致中枢神经系统神经祖细胞系的细胞周期停滞和分化。
Synapse. 2010 Apr;64(4):267-73. doi: 10.1002/syn.20727.
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delta-Opioid receptors protect from anoxic disruption of Na+ homeostasis via Na+ channel regulation.δ-阿片受体通过调节钠离子通道保护细胞免受缺氧导致的钠离子稳态破坏。
Cell Mol Life Sci. 2009 Nov;66(21):3505-16. doi: 10.1007/s00018-009-0136-x.
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Delta opioid agonist [D-Ala2, D-Leu5] enkephalin (DADLE) reduced oxygen-glucose deprivation caused neuronal injury through the MAPK pathway.δ阿片受体激动剂[D-丙氨酸2,D-亮氨酸5]脑啡肽(DADLE)通过丝裂原活化蛋白激酶(MAPK)途径减轻氧糖剥夺引起的神经元损伤。
Brain Res. 2009 Oct 6;1292:100-6. doi: 10.1016/j.brainres.2009.06.104. Epub 2009 Jul 18.
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Hibernation-like state induced by an opioid peptide protects against experimental stroke.阿片肽诱导的类冬眠状态可保护实验性中风。
BMC Biol. 2009 Jun 17;7:31. doi: 10.1186/1741-7007-7-31.
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Na+ mechanism of delta-opioid receptor induced protection from anoxic K+ leakage in the cortex.δ-阿片受体诱导对皮质缺氧性钾离子泄漏产生保护作用的钠离子机制。
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Novel role for the delta-opioid receptor in hypoxic preconditioning in rat retinas.δ-阿片受体在大鼠视网膜缺氧预处理中的新作用。
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Activation of DOR attenuates anoxic K+ derangement via inhibition of Na+ entry in mouse cortex.DOR的激活通过抑制小鼠皮质中Na⁺的内流来减轻缺氧性K⁺紊乱。
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