Endocannabinoids

Hansen, Harald S.; Petersen, Gitte; Artmann, Andreas; Madsen, Andreas Nygaard

doi:10.1002/ejlt.200600157

Cited by 9 publications

(4 citation statements)

References 194 publications

(167 reference statements)

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“…Several possible mechanisms for this action have been suggested including inhibition of phospholipase D (PLDalpha) [15], interaction with phytohormone signaling pathways [16], and modulation of ABI3 transcript levels [17]. However, NAEs have multiple targets in animal systems and perturbation of NAE levels is known to affect a broad range of processes in animals [18]. It is likely that NAE metabolism interacts with several different targets in plant systems, including inhibition of LOX enzymes.…”

Section: Introductionmentioning

confidence: 99%

Lauroylethanolamide is a potent competitive inhibitor of lipoxygenase activity

et al. 2010

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a b s t r a c tThe lipoxygenase (LOX) pathway was proposed to compete with hydrolysis and be partly responsible for the metabolism of polyunsaturated N-acylethanolamines (PU-NAEs). Treatment of Arabidopsis seedlings with lauroylethanolamide (NAE 12:0) resulted in elevated levels of PU-NAE species, and this was most pronounced in plants with reduced NAE hydrolase activity. Enzyme activity assays revealed that NAE 12:0 inhibited LOX-mediated oxidation of PU lipid substrates in a dose-dependent and competitive manner. NAE 12:0 was 10-20 times more potent an inhibitor of LOX activities than lauric acid (FFA 12:0). Furthermore, treatment of intact Arabidopsis seedlings with NAE 12:0 (but not FFA 12:0) substantially blocked the wound-induced formation of jasmonic acid (JA), suggesting that NAE 12:0 may be used in planta to manipulate oxylipin metabolism.

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Section: Introductionmentioning

confidence: 99%

Lauroylethanolamide is a potent competitive inhibitor of lipoxygenase activity

et al. 2010

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“…The endocannabinoid system is a complex signalling system comprised of lipid molecules, enzymes and G-protein coupled receptors responsible for mediating a wide range of effects in organisms such as modifying neurotransmitter release, modulating learning and memory, regulating food intake and modulating inflammation and pain reception [313]. These effects are mediated through the activation of cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2), the latter of which is primarily expressed in the cells of the immune system, including microglia [314,315].…”

Section: Cannabinoidsmentioning

confidence: 99%

Potential pharmacological approaches for the treatment of HIV-1 associated neurocognitive disorders

Omeragic

Kayode

Hoque

et al. 2020

Fluids Barriers CNS

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HIV associated neurocognitive disorders (HAND) are the spectrum of cognitive impairments present in patients infected with human immunodeficiency virus type 1 (HIV-1). The number of patients affected with HAND ranges from 30 to 50% of HIV infected individuals and although the development of combinational antiretroviral therapy (cART) has improved longevity, HAND continues to pose a significant clinical problem as the current standard of care does not alleviate or prevent HAND symptoms. At present, the pathological mechanisms contributing to HAND remain unclear, but evidence suggests that it stems from neuronal injury due to chronic release of neurotoxins, chemokines, viral proteins, and proinflammatory cytokines secreted by HIV-1 activated microglia, macrophages and astrocytes in the central nervous system (CNS). Furthermore, the blood-brain barrier (BBB) not only serves as a route for HIV-1 entry into the brain but also prevents cART therapy from reaching HIV-1 brain reservoirs, and therefore could play an important role in HAND. The goal of this review is to discuss the current data on the epidemiology, pathology and research models of HAND as well as address the potential pharmacological treatment approaches that are being investigated.

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“…Within the past decade, arachidonoylethanolamide (AEA, also called anandamide) and 2‐arachidonoylglycerol (2‐AG) (Fig. 1) have been demonstrated to be agonists for the two known cannabinoid receptors, the CB 1 receptor and the CB 2 receptor (14–16), which are involved in such diverse functions as regulation of food intake, neurotransmitter release, bone formation and pain (17–20). Recently, it has been reported that AEA and 2‐AG also can activate the orphan receptor GPR55 but the biological significance is at present unknown (21).…”

Section: Endocannabinoids Are Derivatives Of Arachidonic Acidmentioning

confidence: 99%

Endocannabinoids and Nutrition

Hansen

Artmann

2008

J Neuroendocrinology

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The endocannabinoids anandamide (AEA) and 2‐arachidonoylglycerol (2‐AG) are bioactive lipids derived from the n‐6 family of polyunsaturated fatty acids that are essential fatty acids. Symptoms of essential fatty acid deficiency in rats – growth retardation, scaly skin, and increased transepidermal water loss – can mainly be attributed to lack of linoleic acid as a structural element of the epidermis. Arachidonic acid, however, also serve essential functions, particularly in cellular signalling via its precursor role for numerous oxygenated derivatives such as prostaglandins, leukotrienes, hepoxilins and other eicosanoids. Furthermore, arachidonic acid is also a structural part of endocannabinoids that have signalling functions in relation to modulation of neurotransmitter release, which might involve physiological and pathophysiological phenomena such as regulation of appetite, energy metabolism, pain perception, memory and learning. Furthermore, along with AEA formation other acylethanolamides are always formed – e.g., oleoylethanolamide (OEA), that can inhibit food intake, and palmitoylethanolamide, that is anti‐inflammatory – possibly through activation of peroxisome proliferator activated receptor α (PPAR α) and/or GPR119. As all these unsaturated fatty acids are ingested daily in smaller or larger amounts, one can ask whether different dietary fats can affect the levels of these fatty acids in the tissues and thereby the quantitative formation of these bioactive signalling molecules. Generally, in vivo arachidonic‐acid‐derived eicosanoid production can be increased and decreased by prolonged feeding with pharmacological levels of arachidonic acid and long‐chain (n‐3) fatty acids (fish oil), respectively. Changes in levels of these two fatty acids within the traditional human diet hardly affects the eicosanoid production, however. Moreover, preliminary data suggest that dietary intake of arachidonic acid and fish oil also doesn’t easily affect endocannabinoid formation; however, dietary fat in terms of saturated, polyunsaturated and monounsaturated seems to affect tissue levels of AEA, 2‐AG and OEA.

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Endocannabinoids

Cited by 9 publications

References 194 publications

Lauroylethanolamide is a potent competitive inhibitor of lipoxygenase activity

Lauroylethanolamide is a potent competitive inhibitor of lipoxygenase activity

Potential pharmacological approaches for the treatment of HIV-1 associated neurocognitive disorders

Endocannabinoids and Nutrition

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