RT Journal Article
T1 Systemic administration of oleoylethanolamide protects from neuroinflammation and anhedonia induced by LPS in rats.
A1 Sayd, Aline
A1 Antón, María
A1 Alén, Francisco
A1 Caso, Javier Rubén
A1 Pavón, Javier
A1 Leza, Juan Carlos
A1 Rodríguez de Fonseca, Fernando
A1 García-Bueno, Borja
A1 Orio, Laura
K1 OLEA
K1 Lipopolysaccharide
K1 Neuroinflammation
K1 Anhedonia
K1 Antiinflamatorios
K1 Corticosterona
K1 Citocinas
K1 Modelos de enfermedad en animales
K1 Encefalitis
K1 Endocannabinoides
K1 Endotoxinas
K1 Etanolaminas
K1 PEA
K1 Preferencias alimenticias
K1 Lóbulo frontal
K1 Sistema hipotálamo-hipofisario
K1 Mediadores de la inflamación
K1 Peroxidación de lípidos
K1 Fármacos neuroprotectores
K1 Ácidos oleicos
K1 Estrés oxidativo
K1 Ácidos palmíticos
K1 Sistema hipófiso-suprarrenal
K1 Ratas wistar
K1 Percepción del gusto
AB BACKGROUNDThe acylethanolamides oleoylethanolamide and palmitoylethanolamide are endogenous lipid mediators with proposed neuroprotectant properties in central nervous system (CNS) pathologies. The precise mechanisms remain partly unknown, but growing evidence suggests an antiinflammatory/antioxidant profile.METHODSWe tested whether oleoylethanolamide/palmitoylethanolamide (10 mg/kg, i.p.) attenuate neuroinflammation and acute phase responses (hypothalamus-pituitary-adrenal (HPA) stress axis stress axis activation, thermoregulation, and anhedonia) induced by lipopolysaccharide (0.5 mg/kg, i.p.) in rats.RESULTSLipopolysaccharide increased mRNA levels of the proinflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6, nuclear transcription factor-κB activity, and the expression of its inhibitory protein IκBα in cytoplasm, the inducible isoforms of nitric oxide synthase and cyclooxygenase-2, microsomal prostaglandin E2 synthase mRNA, and proinflammatory prostaglandin E2 content in frontal cortex 150 minutes after administration. As a result, the markers of nitrosative/oxidative stress nitrites (NO2(-)) and malondialdehyde were increased. Pretreatment with oleoylethanolamide/ palmitoylethanolamide reduced plasma tumor necrosis factor-α levels after lipopolysaccharide, but only oleoylethanolamide significantly reduced brain tumor necrosis factor-α mRNA. Oleoylethanolamide and palmitoylethanolamide prevented lipopolysaccharide-induced nuclear transcription factor-κB (NF-κB)/IκBα upregulation in nuclear and cytosolic extracts, respectively, the expression of inducible isoforms of nitric oxide synthase, cyclooxygenase-2, and microsomal prostaglandin E2 synthase and the levels of prostaglandin E2. Additionally, both acylethanolamides reduced lipopolysaccharide-induced oxidative/nitrosative stress. Neither oleoylethanolamide nor palmitoylethanolamide modified plasma corticosterone levels after lipopolysaccharide, but both acylethanolamides reduced the expression of hypothalamic markers of thermoregulation interleukin-1β, cyclooxygenase-2, and prostaglandin E2, and potentiated the hypothermic response after lipopolysaccharide. Interestingly, only oleoylethanolamide disrupted lipopolysaccharide-induced anhedonia in a saccharine preference test.CONCLUSIONSResults indicate that oleoylethanolamide and palmitoylethanolamide have antiinflammatory/neuroprotective properties and suggest a role for these acylethanolamides as modulators of CNS pathologies with a neuroinflammatory component.
PB Oxford University Press
SN 1461-1457
YR 2015
FD 2015-04
LK http://hdl.handle.net/10668/2337
UL http://hdl.handle.net/10668/2337
LA en
NO Said A, Antón M, Alén F, Caso JR, Pavón  J, Leza JC, et al. Systemic Administration of Oleoylethanolamide Protects from Neuroinflammation and Anhedonia Induced by LPS in Rats. Int J Neuropsychopharmacol. 2015; 18 (6). pyu111.
NO Comparative Study; Journal Article; Research Support, Non-U.S. Gov't;Erratium: http://ijnp.oxfordjournals.org/content/19/3/pyw004.long
DS RISalud
RD Apr 11, 2025