Involvement of the cannabimimetic compound, N-palmitoyl-ethanolamine, in inflammatory and neuropathic conditions: Review of the available pre-clinical data, and first human studies

Darmani, Nissar A.; Izzo, Angelo A.; Degenhardt, Brian F.; Valenti, Marta; Scaglione, Giuseppe; Capasso, Raffaele; Sorrentini, I.; Marzo, Vincenzo Di

doi:10.1016/j.neuropharm.2005.01.001

Cited by 132 publications

(91 citation statements)

References 74 publications

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“…Indeed, anandamide and N-palmitoylethanolamine levels are altered in colon mucosal biopsies of patients with ulcerative colitis (UC) or Crohn's disease (CD), especially during acute flares, with no change in 2-arachidonoylglycerol levels [35,52,53] (changes in the ECS in human IBD are summarized in Table 1). NAE levels were reported to be either increased or decreased depending on the study.…”

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confidence: 99%

The endocannabinoid system in inflammatory bowel diseases: from pathophysiology to therapeutic opportunity

Alhouayek

Muccioli

2012

Trends in Molecular Medicine

119

100

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Section: Box 2 the Ecs Toolboxmentioning

confidence: 99%

The endocannabinoid system in inflammatory bowel diseases: from pathophysiology to therapeutic opportunity

Alhouayek

Muccioli

2012

Trends in Molecular Medicine

119

100

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“…PEA treatment in animals has demonstrated the efficacy of and great promise for its use in the treatment of neuropathic, inflammatory (3 -6), and postoperative pain (7). These effects of PEA may occur through several possible mechanisms (8).…”

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confidence: 99%

N-Palmitoyl-ethanolamine (PEA) Induces Peripheral Antinociceptive Effect by ATP-Sensitive K+-Channel Activation

Romero

Duarte

2012

J Pharmacol Sci

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“…PEA is endowed with antiallergic, anti-inflammatory, and antinociceptive properties (Calignano et al, 1998) and may elicit a wide range of in vivo effects that includes analgesia, inhibition of food intake, reduction of gastrointestinal motility, inhibition of cancer cell proliferation, and cytoprotection (Lambert and Di Marzo, 1999). Under physiological conditions, PEA is present at high concentrations in the central nervous system (Cadas et al, 1997), where its concentrations significantly increase under pathological conditions, like brain ischemia (Franklin et al, 2003;Berger et al, 2004), excitotoxicity (Di Marzo et al, 1994;Hansen et al, 1995), and neuroinflammation (Darmani et al, 2005). In vitro and in vivo experiments suggest that PEA has neuroprotective activity; it protects cerebellar granule neurons against excitotoxicity (Skaper et al, 1996), inhibits electroshock-and chemically induced seizures in mice (Sheerin et al, 2004), and enhances microglial cell motility (Franklin et al, 2003).…”

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Oxyhomologation of the Amide Bond Potentiates Neuroprotective Effects of the EndolipidN-Palmitoylethanolamine

Lombardi¹,

Miglio²,

Varsaldi³

et al. 2006

J Pharmacol Exp Ther

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The endolipid N-palmitoylethanolamine (PEA) shows a pleiotropic pattern of bioactivities, whose mechanistic characterization is still unclear and whose pharmacological potential is substantially limited by rapid metabolization by the amido hydrolyzing enzymes fatty acid amide hydrolases and N-acylethanolaminehydrolyzing acid amidase. To overcome this problem, we have synthesized a new series of PEA homologs and characterized their activity on two in vitro models of neurodegeneration (oxidative stress, excitotoxicity). PEA partially prevented tert-butylhydroperoxide (t-BOOH; 100 M; 3 h)-induced cell death (maximal effect, 26.3 Ϯ 7.5% in comparison with t-BOOHuntreated cells at 30 M), whereas it was ineffective against the L-glutamate (1 mM; 24 h)-induced excitotoxicity at all concentrations tested (0.01-30 M). Oxyhomologation of the amide bond, although leading to an increased enzymatic stability, also potentiated neuroprotective activity, especially for N-palmitoyl-N-(2-hydroxyethyl)hydroxylamine (EC 50 ϭ 2.1 M). These effects were not mediated by cannabinoid/vanilloid-dependent mechanisms but rather linked to a decreased t-BOOH-induced lipoperoxidation and reactive oxygen species formation and L-glutamate-induced intracellular Ca 2ϩ overload. The presence of the hydroxamic group and the absence of either redox active or radical scavenger moieties suggest that the improved neuroprotection is the result of increased metal-chelating properties that boost the antioxidant activity of these compounds.

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Involvement of the cannabimimetic compound, N-palmitoyl-ethanolamine, in inflammatory and neuropathic conditions: Review of the available pre-clinical data, and first human studies

Cited by 132 publications

References 74 publications

The endocannabinoid system in inflammatory bowel diseases: from pathophysiology to therapeutic opportunity

The endocannabinoid system in inflammatory bowel diseases: from pathophysiology to therapeutic opportunity

N-Palmitoyl-ethanolamine (PEA) Induces Peripheral Antinociceptive Effect by ATP-Sensitive K+-Channel Activation

Oxyhomologation of the Amide Bond Potentiates Neuroprotective Effects of the EndolipidN-Palmitoylethanolamine

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