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Molecular Neurodegeneration BioMed
Research article
The neuroprotective properties of palmitoylethanolamine against
oxidative stress in a neuronal cell line
R Scott Duncan* , Kent D Chapman2,3 and Peter Koulen1,3
Address: 'Departments of Basic Medical Science and Ophthalmology, University of Missouri - Kansas City, 2411 Holmes St, Kansas City, MO
64108-2792, USA, 2Department of Biological Sciences, University of North Texas, 1155 Union Circle, #305220, Denton, TX 76203-5217, USA and
3Center for Plant Lipid Research, University of North Texas, 1155 Union Circle, #305220, Denton, TX 76203-5217, USA
Email: R Scott Duncan* - duncanrs@umkc.edu; Kent D Chapman - chapman@unt.edu; Peter Koulen - koulenp@umkc.edu
* Corresponding authorPublished: 10 December 2009
Molecular Neurodegeneration 2009, 4:50 doi: 10. 1186/1750-1 326-4-50Received: 15 July 2009
Accepted: 10 December 2009This article is available from: http://www.molecularneurodegeneration.com/content/4/1/50
@ 2009 Duncan et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background: N-acylethanolamines (NAEs) are lipids upregulated in response to cell and tissue
injury and are involved in cytoprotection. Arachidonylethanolamide (AEA) is a well characterized
NAE that is an endogenous ligand at cannabinoid and vanilloid receptors, but it exists in small
quantities relative to other NAE types. The abundance of other NAE species, such as
palmitoylethanolamine (PEA), together with their largely unknown function and receptors, has
prompted us to examine the neuroprotective properties and mechanism of action of PEA. We
hypothesized that PEA protects HT22 cells from oxidative stress and activates neuroprotective
kinase signaling pathways.
Results: Indeed PEA protected HT22 cells from oxidative stress in part by mediating an increase
in phosphorylated Akt (pAkt) and ERK I/2 immunoreactivity as well as pAkt nuclear translocation.
These changes take place within a time frame consistent with neuroprotection. Furthermore, we
determined that changes in pAkt immunoreactivity elicited by PEA were not mediated by activation
of cannabinoid receptor type 2 (CB2), thus indicating a novel mechanism of action. These results
establish a role for PEA as a neuroprotectant against oxidative stress, which occurs in a variety of
neurodegenerative diseases.
Conclusions: The results from this study reveal that PEA protects HT22 cells from oxidative
stress and alters the localization and expression levels of kinases known to be involved in
neuroprotection by a novel mechanism. Overall, these results identify PEA as a neuroprotectant
with potential as a possible therapeutic agent in neurodegenerative diseases involving oxidative
stress.Introduction
N-Acylethanolamines (NAEs) are endogenous lipids
involved in cell signaling and they are synthesized in
response to cellular injury [1,2]. The NAE, arachido-
nylethanolamide (AEA), is a cannabinoid exhibiting cyto-
protective properties against a wide variety of pathologicalinsults including excitotoxicity, oxidative stress and
hypoxia [3-10]. Cannabinoids activate the G-protein-cou-
pled cannabinoid receptors (CB1 and CB2) leading to
downregulation of PKA and activation of the ERK MAPK
pathway, a neuroprotective signaling pathway [11-18].
Furthermore, the activation of Akt by cannabinoids fur-Page 1 of 12
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Duncan, Scott R.; Chapman, Kent D. & Koulen, Peter. The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line, article, December 10, 2009; [London, United Kingdom]. (https://digital.library.unt.edu/ark:/67531/metadc122166/m1/1/: accessed July 18, 2024), University of North Texas Libraries, UNT Digital Library, https://digital.library.unt.edu; crediting UNT College of Arts and Sciences.