Abstract
Several fatty acid derivatives capable of either directly activating the cannabinoid receptors (CBRs) or exerting cannabimimetic effects have been identified. These are the endogenous ligands of CBRs, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), and the AEA congener, palmitoylethanolamide (PEA) (see [1,2] for reviews). The biosynthesis of AEA, PEA, and 2-AG can be induced by stimulation with either Ca2+ionophores, lipopolysaccharide or platelet activating factor in macrophages, and by ionomycin or antigen challenge in rat basophilic leukemia (RBL-2H3) cells (3,4). These cells also inactivate AEA, PEA and 2-AG through re-uptake and/or hydrolysis and/or esterification processes (5,6). AEA and PEA modulate cytokine and/or arachidonate release from macrophages in vitro, regulate serotonin secretion from RBL-2H3 cells, and are analgesic in some animal models of inflammatory pain. However, the involvement of theendogenousmetabolites and of cannabinoid CB1and CB2receptors in these effects is still controversial (see [7] for review).KeywordsNerve Growth FactorHuman Breast Cancer CellFatty Acid DerivativeProstate Cancer Cell ProliferationHigh Affinity Nerve Growth FactorThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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