摘要
经典的内源性大麻素(CB)系统由神经信号分子,2-arachidonoyl甘油(2-AG)和叫花生四烯酸乙醇胺(AEA)及其受体(GPCR),g蛋白耦合CB1和CB2构成神经系统(ECS)。然而,假定的,最新的lipid-sensing CB受体最近被确认,包括孤儿GPR55和GPR18受体受到cannabinoid-like分子和与CB体系。CB受体和相关的孤儿GPCRs表达高水平的免疫和/或中枢神经系统(CNS)和调节的神经生理学过程,包括关键事件参与神经炎症。因此,这些受体被确认为新兴治疗靶点的脑部疾病的存在是一个关键的功能,包括多发性硬化症(MS)和阿尔茨海默病(AD)。本文将考虑更广泛的大麻素受体的作用在调节免疫功能总科重点是免疫过程,有助于神经炎症条件。
关键词: 大麻素. 神经的. GPR55. GPR18. 炎症. 神经炎症. 神经退化
图形摘要
Current Drug Targets
Title:The Emerging Role of the Cannabinoid Receptor Family in Peripheral and Neuro-immune Interactions
Volume: 17 Issue: 16
Author(s): Orla Haugh, June Penman, Andrew J. Irving, Veronica A. Campbell
Affiliation:
关键词: 大麻素. 神经的. GPR55. GPR18. 炎症. 神经炎症. 神经退化
摘要: The classical endogenous cannabinoid (CB) system is composed of the endocannabinoid signalling molecules, 2-arachidonoyl glycerol (2-AG) and anandamide (AEA) and their G-protein coupled receptors (GPCR), CB1 and CB2 which together constitutes the endocannabinoid system (ECS). However, putative, novel lipid-sensing CB receptors have recently been identified, including the orphan GPR55 and GPR18 receptors that are regulated by cannabinoid-like molecules and interact with CB system. CB receptors and associated orphan GPCRs are expressed at high levels in the immune and/or central nervous systems (CNS) and regulate a number of neurophysiological processes, including key events involved in neuroinflammation. As such, these receptors have been identified as emerging therapeutic targets for a number of brain disorders in which neuroinflammation is a key feature, including multiple sclerosis (MS) and Alzheimer’s disease (AD). This review will consider the role of the wider cannabinoid receptor superfamily in mediating immune function with a focus on the immune processes that contribute to neuroinflammatory conditions.
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Cite this article as:
Orla Haugh, June Penman, Andrew J. Irving, Veronica A. Campbell , The Emerging Role of the Cannabinoid Receptor Family in Peripheral and Neuro-immune Interactions, Current Drug Targets 2016; 17 (16) . https://dx.doi.org/10.2174/1389450117666160112113703
DOI https://dx.doi.org/10.2174/1389450117666160112113703 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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