Putative neuroprotective actions of N-acyl-ethanolamines

被引:60
作者
Hansen, HS [1 ]
Moesgaard, B [1 ]
Petersen, G [1 ]
Hansen, HH [1 ]
机构
[1] Royal Danish Sch Pharm, Dept Pharmacol, DK-2100 Copenhagen, Denmark
关键词
N-acyl-ethanolamine phospholipids; anandamide; neurodegeneration; ischemia; brain; necrosis;
D O I
10.1016/S0163-7258(02)00251-6
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
N-Acyl-ethanotamines (NAEs) and their precursors, N-acyl-ethanolamine phospholipids (NAPEs), are present in the mammalian brain at levels of a few hundred picomoles/gram tissue and a few nanomoles/gram tissue, respectively. NAE-containing arachidonic acid is called anandamide, and it has attracted particular attention since it is a partial agonist for the cannabinoid receptors, for which 2-arachidonoylglycerol is the full agonist. In addition, anandamide may also activate the vanilloid receptor. Anandamide usually amounts to 1-10% of NAEs, as the vast majority of N-acyl groups are saturated and monounsaturated fatty acids. Formation of NAPE and NAE is catalyzed by an N-acyltransferase and an NAPE-hydrolyzing phospholipase D. respectively, two enzymes that have been characterized only preliminary. Interestingly, NAPEs and NAEs accumulate in the brain in response to neurodegenerative insults at a time when other phospholipids are subjected to rapid degradation. This is an important biosynthetic aspect of NAPE and NAE, as NAEs may be neuroprotective by a number of different mechanisms involving both receptor activation and non-receptor-mediated effects, e.g. by binding to cannabinoid receptors and interfering with ceramide turnover, respectively. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:119 / 126
页数:8
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