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

@article{Darmani2005InvolvementOT,
  title={Involvement of the cannabimimetic compound, N-palmitoyl-ethanolamine, in inflammatory and neuropathic conditions: Review of the available pre-clinical data, and first human studies},
  author={Nissar A. Darmani and Angelo A. Izzo and Brian F. Degenhardt and Marta Valenti and Giuseppe Scaglione and Raffaele Capasso and Italo Sorrentini and Vincenzo Di Marzo},
  journal={Neuropharmacology},
  year={2005},
  volume={48},
  pages={1154-1163}
}

Figures and Tables from this paper

Anti-Inflammatory, Antioxidant and Crystallographic Studies of N-Palmitoyl-Ethanol Amine (PEA) Derivatives
TLDR
Biological evaluation of a small library of N-palmitoyl-ethanolamine analogues or derivatives, characterized by a protected acid function, useful to decrease their hydrolysis rate in vitro and prolong their biological activity are reported.
The pharmacology of palmitoylethanolamide and first data on the therapeutic efficacy of some of its new formulations
TLDR
An overview of the pharmacology, efficacy and safety of PEA in neurodegenerative disorders, pain perception and inflammatory diseases is provided.
Care and Feeding of the Endocannabinoid System: A Systematic Review of Potential Clinical Interventions that Upregulate the Endocannabinoid System
TLDR
Evidence indicates that several classes of pharmaceuticals upregulate the eCB system, including analgesics, non-steroidal anti-inflammatory drugs, opioids, glucocorticoids, antidepressants, antipsychotics, anxiolytics, and anticonvulsants.
N-palmitoyl-ethanolamine (PEA) induces peripheral antinociceptive effect by ATP-sensitive K+-channel activation.
TLDR
Results indicate that the activation of ATP-sensitive K(+) channels could be the mechanism that induces peripheral antinociception by PEA and that voltage-dependent K(+ channels and small and large conductance Ca(2+)-activated K(-) channels do not appear to be involved in this mechanism.
Effect of Ultra-Micronized-Palmitoylethanolamide and Acetyl-l-Carnitine on Experimental Model of Inflammatory Pain
TLDR
Findings showed the superior anti-inflammatory and anti-nociceptive action displayed by oral administration of um-PEA and LAC versus LAC plus, separate but consecutive, um- PEA in the rat paw CAR model of inflammatory pain.
Effects of the FAAH inhibitor, URB597, and anandamide on lithium-induced taste reactivity responses: a measure of nausea in the rat
TLDR
The results suggest that prolonging the action of anandamide by pretreatment with the FAAH inhibitor, URB597, suppresses lithium-induced nausea in the rat.
...
...

References

SHOWING 1-10 OF 84 REFERENCES
The palmitoylethanolamide family: a new class of anti-inflammatory agents?
TLDR
In the present review, the biochemical and pharmacological properties of PEA are discussed, in particular with respect to its analgesic and anti-inflammatory properties.
Antiinflammatory action of endocannabinoid palmitoylethanolamide and the synthetic cannabinoid nabilone in a model of acute inflammation in the rat
TLDR
The antiinflammatory effect of nabilone is shown and that of palmitoylethanolamide is confirmed indicating that these actions are mediated by an uncharacterized CB2‐like cannabinoid receptor.
Putative neuroprotective actions of N-acyl-ethanolamines.
Therapeutic effect of the endogenous fatty acid amide, palmitoylethanolamide, in rat acute inflammation: inhibition of nitric oxide and cyclo‐oxygenase systems
TLDR
It is shown, for the first time, that palmitoylethanolamide has a curative effect in a model of acute inflammation, inhibiting the carrageenan‐induced oedema in a dose‐ and time‐dependent manner.
Antinociceptive activity of the endogenous fatty acid amide, palmitylethanolamide.
...
...