The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line

<p>Abstract</p> <p>Background</p> <p>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 van...

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Main Authors: Chapman Kent D, Duncan R Scott, Koulen Peter
Format: Article
Language:English
Published: BMC 2009-12-01
Series:Molecular Neurodegeneration
Online Access:http://www.molecularneurodegeneration.com/content/4/1/50
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spelling doaj-107528ae327146de9a6d1271a277aef62020-11-25T00:36:52ZengBMCMolecular Neurodegeneration1750-13262009-12-01415010.1186/1750-1326-4-50The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell lineChapman Kent DDuncan R ScottKoulen Peter<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Results</p> <p>Indeed PEA protected HT22 cells from oxidative stress in part by mediating an increase in phosphorylated Akt (pAkt) and ERK1/2 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.</p> <p>Conclusions</p> <p>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.</p> http://www.molecularneurodegeneration.com/content/4/1/50
collection DOAJ
language English
format Article
sources DOAJ
author Chapman Kent D
Duncan R Scott
Koulen Peter
spellingShingle Chapman Kent D
Duncan R Scott
Koulen Peter
The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line
Molecular Neurodegeneration
author_facet Chapman Kent D
Duncan R Scott
Koulen Peter
author_sort Chapman Kent D
title The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line
title_short The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line
title_full The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line
title_fullStr The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line
title_full_unstemmed The neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line
title_sort neuroprotective properties of palmitoylethanolamine against oxidative stress in a neuronal cell line
publisher BMC
series Molecular Neurodegeneration
issn 1750-1326
publishDate 2009-12-01
description <p>Abstract</p> <p>Background</p> <p>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.</p> <p>Results</p> <p>Indeed PEA protected HT22 cells from oxidative stress in part by mediating an increase in phosphorylated Akt (pAkt) and ERK1/2 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.</p> <p>Conclusions</p> <p>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.</p>
url http://www.molecularneurodegeneration.com/content/4/1/50
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