A co-ultramicronized palmitoylethanolamide/luteolin composite mitigates clinical score and disease-relevant molecular markers in a mouse model of experimental autoimmune encephalomyelitis.
EAE, Acute phase response
Multiple sclerosis
PEALut
Journal
Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974
Informations de publication
Date de publication:
20 Jun 2019
20 Jun 2019
Historique:
received:
31
01
2019
accepted:
04
06
2019
entrez:
22
6
2019
pubmed:
22
6
2019
medline:
14
1
2020
Statut:
epublish
Résumé
Persistent and/or recurrent inflammatory processes are the main factor leading to multiple sclerosis (MS) lesions. The composite ultramicronized palmitoylethanolamide, an endogenous N-acylethanolamine, combined with the flavonoid luteolin, PEALut, have been found to exert neuroprotective activities in experimental models of spinal and brain injury and Alzheimer disease, as well as a clinical improvement in human stroke patients. Furthermore, PEALut enhances the expression of different myelin proteins in oligodendrocyte progenitor cells suggesting that this composite might have protective effects in MS experimental models. The mouse model of experimental autoimmune encephalomyelitis (EAE) based on active immunization with a fragment of myelin oligodendrocyte glycoprotein (MOG Vehicle-MOG The present results demonstrate that the intraperitoneal administration of the composite PEALut significantly reduces the development of clinical signs in the MOG
Sections du résumé
BACKGROUND
BACKGROUND
Persistent and/or recurrent inflammatory processes are the main factor leading to multiple sclerosis (MS) lesions. The composite ultramicronized palmitoylethanolamide, an endogenous N-acylethanolamine, combined with the flavonoid luteolin, PEALut, have been found to exert neuroprotective activities in experimental models of spinal and brain injury and Alzheimer disease, as well as a clinical improvement in human stroke patients. Furthermore, PEALut enhances the expression of different myelin proteins in oligodendrocyte progenitor cells suggesting that this composite might have protective effects in MS experimental models.
METHODS
METHODS
The mouse model of experimental autoimmune encephalomyelitis (EAE) based on active immunization with a fragment of myelin oligodendrocyte glycoprotein (MOG
RESULTS
RESULTS
Vehicle-MOG
CONCLUSIONS
CONCLUSIONS
The present results demonstrate that the intraperitoneal administration of the composite PEALut significantly reduces the development of clinical signs in the MOG
Identifiants
pubmed: 31221190
doi: 10.1186/s12974-019-1514-4
pii: 10.1186/s12974-019-1514-4
pmc: PMC6587257
doi:
Substances chimiques
Amides
0
Biomarkers
0
Cytokines
0
Ethanolamines
0
Neuroprotective Agents
0
Palmitic Acids
0
palmidrol
6R8T1UDM3V
Luteolin
KUX1ZNC9J2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
126Références
Amyloid. 2000 Jun;7(2):105-10
pubmed: 10842712
Synapse. 2001 Sep 1;41(3):195-202
pubmed: 11391780
FASEB J. 2001 Oct;15(12):2241-6
pubmed: 11641251
Brain Pathol. 2002 Jul;12(3):308-19
pubmed: 12146799
Brain Res. 2006 Aug 30;1107(1):199-205
pubmed: 16822488
J Immunol. 2009 Jul 15;183(2):787-91
pubmed: 19570822
Exp Neurol. 2010 Jul;224(1):48-55
pubmed: 20353771
J Neurosci. 2012 Dec 12;32(50):18246-52
pubmed: 23238738
Pain. 2013 Dec;154 Suppl 1:S87-93
pubmed: 23623250
CNS Neurol Disord Drug Targets. 2013 Nov;12(7):989-1001
pubmed: 23844686
Inflammopharmacology. 2014 Apr;22(2):79-94
pubmed: 24178954
Mult Scler. 2014 Mar;20(3):271-9
pubmed: 24589684
Pharmacol Res. 2014 Aug;86:32-41
pubmed: 24844438
J Neurotrauma. 2016 Jan 1;33(1):132-46
pubmed: 25046306
CNS Neurol Disord Drug Targets. 2014;13(9):1530-41
pubmed: 25106636
Neurology. 2014 Sep 9;83(11):1022-4
pubmed: 25200713
Neuroscience. 2015 Apr 2;290:279-87
pubmed: 25637488
Brain Res Bull. 2015 Oct;119(Pt A):1-11
pubmed: 26361743
Sci Rep. 2015 Nov 18;5:16676
pubmed: 26578323
Transl Stroke Res. 2016 Feb;7(1):54-69
pubmed: 26706245
Pain Physician. 2016 Feb;19(2):11-24
pubmed: 26815246
Front Pharmacol. 2016 Mar 08;7:47
pubmed: 27014061
J Neuroinflammation. 2016 Jun 03;13(1):136
pubmed: 27256343
Pharmacol Ther. 2016 Oct;166:40-55
pubmed: 27373505
Br J Pharmacol. 2017 Jun;174(11):1349-1365
pubmed: 27539936
Brain Res. 2017 Jan 1;1654(Pt A):55-65
pubmed: 27608955
Physiol Rev. 2016 Oct;96(4):1593-659
pubmed: 27630175
Brain Pathol. 2017 Mar;27(2):213-219
pubmed: 27997058
Br J Pharmacol. 2017 Jul;174(14):2393-2408
pubmed: 28471519
Front Neurol. 2017 Jun 06;8:233
pubmed: 28634464
Mol Neurobiol. 2018 Jan;55(1):103-114
pubmed: 28822061
Adv Pharmacol. 2017;80:291-328
pubmed: 28826538
Sci Rep. 2017 Sep 22;7(1):12158
pubmed: 28939905
J Neuroinflammation. 2017 Sep 30;14(1):196
pubmed: 28964257
Prog Neurobiol. 2018 Jan;160:82-100
pubmed: 29097192
Eur J Med Chem. 2017 Dec 1;141:703-720
pubmed: 29102463
Methods Mol Biol. 2018;1727:353-360
pubmed: 29222794
Mol Neurobiol. 2018 Aug;55(8):6894-6905
pubmed: 29357041
Lancet. 2018 Apr 21;391(10130):1622-1636
pubmed: 29576504
Front Pharmacol. 2018 Mar 20;9:249
pubmed: 29615912
Life Sci. 2018 Jul 1;204:20-45
pubmed: 29729263
J Mol Neurosci. 2018 Aug;65(4):491-506
pubmed: 30083786
Nat Rev Drug Discov. 2018 Sep;17(9):623-639
pubmed: 30116049
Front Mol Neurosci. 2018 Sep 04;11:320
pubmed: 30233319
Immunol Today. 1994 Feb;15(2):74-80
pubmed: 7512342
J Neuroimmunol. 1998 Aug 1;88(1-2):9-12
pubmed: 9688318
J Histochem Cytochem. 1998 Dec;46(12):1377-84
pubmed: 9815279