Search results for "arachidonic"

showing 10 items of 178 documents

Cell mechanisms of gustatory lipids perception and modulation of the dietary fat preference.

2014

Dietary lipids are usually responsible of several metabolic disorders. Recent compelling evidences suggest that there is a sixth taste modality, destined for the detection of oro-gustatory fats. The lipid-binding glycoprotein CD36, expressed by circumvallate papillae (CVP) of the mouse tongue, has been shown to be implicated in oro-gustatory perception of dietary lipids. We demonstrate that linoleic acid (LA) by activating sPLA2, cPLA2 and iPLA2 via CD36, produced arachidonic acid (AA) and lyso-phosphatidylcholine (Lyso-PC) which triggered Ca(2+) influx in CD36-positive taste bud cells (TBC), purified from mouse CVP. LA induced the production of Ca(2+) influx factor (CIF). CIF, AA and Lyso-…

CD36 AntigensTasteCD36Linoleic acidBiochemistryModels Biologicalchemistry.chemical_compoundFood PreferencesAnimalsHumansStromal Interaction Molecule 1Calcium signalingbiologyORAI1Endoplasmic reticulumMembrane ProteinsTaste PerceptionSTIM1General MedicineTaste BudsDietary FatsCell biologyNeoplasm ProteinschemistryBiochemistrybiology.proteinArachidonic acidCalciumBiochimie
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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB(1)).

2012

Endocannabinoids exert numerous effects in the CNS under physiological and pathological conditions. The aim of the present study was to examine whether the endocannabinoid N-arachidonoyldopamine (NADA) may protect neurons in excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). OHSC were excitotoxically lesioned by application of N-methyl-d-aspartate (NMDA, 50 μM) for 4 h and subsequently treated with different NADA concentrations (0.1 pM-50 μM) alone or in combination with cannabinoid receptor antagonists. NADA protected dentate gyrus granule cells and caused a slight reduction in the number of microglial cells. The number of degenerated neurons significantly decreased be…

Cannabinoid receptorDopamineTRPV1Arachidonic AcidsPharmacologyNeuroprotectionHippocampusCellular and Molecular NeuroscienceMicePiperidinesReceptor Cannabinoid CB1Neuronal damageAnimalsRats WistarCells CulturedPharmacologyNeuronsChemistryDentate gyrusExcitatory Postsynaptic PotentialsEndocannabinoid systemRatsNeuroprotective Agentsnervous systemNerve DegenerationCannabinoid receptor antagonistNMDA receptorPyrazolesNeuropharmacology
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Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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Insulin-like growth factors counteract the effect of interleukin 1 beta on type II phospholipase A2 expression and arachidonic acid release by rabbit…

1994

International audience; Interleukin 1 beta was found to stimulate arachidonic acid release, and the synthesis and secretion of type II phospholipase A2 by rabbit articular chondrocytes in vitro. Interleukin 1 beta had no effect on the level of cytosolic phospholipase A2 mRNA. Insulin-like growth factors, which help stabilize the cartilage matrix, reduced the effect of interleukin 1 beta on type II phospholipase A2 activity and mRNA level, and decreased the Interleukin 1 beta-stimulated arachidonic acid release to the basal values. This suggests that type II phospholipase A2 plays a key role in arachidonic acid release from rabbit articular chondrocytes and that insulin-like growth factors c…

Cartilage Articularmedicine.medical_specialtymedicine.medical_treatmentBiophysicsIn Vitro TechniquesBiochemistryChondrocytePhospholipases AInterleukin 1βInsulin-like growth factorchemistry.chemical_compoundPhospholipase A2[ CHIM.ORGA ] Chemical Sciences/Organic chemistryPhospholipase A2Structural BiologyInsulin-Like Growth Factor IIInternal medicineGeneticsmedicineAnimalsInsulin-like growth factorRNA MessengerInsulin-Like Growth Factor IMolecular BiologyArachidonic Acidbiology[CHIM.ORGA]Chemical Sciences/Organic chemistryArthritisInterleukinCell Biology[CHIM.ORGA] Chemical Sciences/Organic chemistryChondrocyteSomatomedinPhospholipases A2Endocrinologymedicine.anatomical_structureCytokinechemistryInsulin-like growth factor 2biology.proteinArachidonic acidRabbitsInterleukin-1
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Hypersusceptibility of neutrophil granulocytes towards lethal action of free fatty acids contained in enzyme-modified atherogenic low density lipopro…

2008

Abstract Objective The bulk of LDL entrapped in the arterial intima is modified by hydrolytic enzymes, leading to extensive cleavage of cholesterylesters and liberation of fatty acids. The latter induce apoptosis in endothelial cells but are far less cytotoxic towards macrophages. We have compared the cytotoxic effects of enzymatically modified LDL (E-LDL) on macrophages and polymorphonuclear granulocytes (PMN). Methods and results E-LDL displayed toxicity towards PMN at far lower concentrations than towards monocyte-derived macrophages. Native or oxidized LDL had no effect. Free fatty acids contained in E-LDL were the cause of the observed toxicity, which could be mimicked by linoleic acid…

Cell Membrane PermeabilityTime FactorsCell SurvivalNeutrophilsLinoleic acidGranulocyteFatty Acids NonesterifiedHemolysisLinoleic Acidchemistry.chemical_compoundAdenosine TriphosphateSuperoxidesmedicineAnimalsHumansPropidium iodideCells CulturedPeroxidaseRespiratory BurstArachidonic AcidCell DeathL-Lactate DehydrogenaseSuperoxideHydrolysisMacrophagesSterol EsteraseAtherosclerosisRespiratory burstLipoproteins LDLOleic acidmedicine.anatomical_structurechemistryBiochemistryLow-density lipoproteinlipids (amino acids peptides and proteins)Arachidonic acidCalciumRabbitsCardiology and Cardiovascular MedicineOleic AcidPeptide HydrolasesAtherosclerosis
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Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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Neuronal Activity Drives Localized Blood-Brain-Barrier Transport of Serum Insulin-like Growth Factor-I into the CNS

2010

Upon entry into the central nervous system (CNS), serum insulin-like growth factor-1 (IGF-I) modulates neuronal growth, survival, and excitability. Yet mechanisms that trigger IGF-I entry across the blood-brain barrier remain unclear. We show that neuronal activity elicited by electrical, sensory, or behavioral stimulation increases IGF-I input in activated regions. Entrance of serum IGF-I is triggered by diffusible messengers (i.e., ATP, arachidonic acid derivatives) released during neurovascular coupling. These messengers stimulate matrix metalloproteinase-9, leading to cleavage of the IGF binding protein-3 (IGFBP-3). Cleavage of IGFBP-3 allows the passage of serum IGF-I into the CNS thro…

Central Nervous SystemTime FactorsMicrodialysismedicine.medical_treatmentAction PotentialsStimulationFunctional LateralityBody TemperatureReceptor IGF Type 1chemistry.chemical_compoundNeural PathwaysPremovement neuronal activityDrug InteractionsInsulin-Like Growth Factor IMicroscopy ImmunoelectronReceptorCells CulturedNeuronsGeneral NeuroscienceSysneuro//purl.org/becyt/ford/3.1 [https]Protein TransportMedicina Básicamedicine.anatomical_structureMatrix Metalloproteinase 9Blood-Brain BarrierSIGNALING//purl.org/becyt/ford/3 [https]Arachidonic acidNeurogliaLow Density Lipoprotein Receptor-Related Protein-1CIENCIAS MÉDICAS Y DE LA SALUDNeuroscience(all)Central nervous systemNeurocienciasBiophysicsGlutamic AcidEnzyme-Linked Immunosorbent AssayNerve Tissue ProteinsBiologyBlood–brain barrierMOLNEUROmedicineAnimalsHumansImmunoprecipitationRats WistarAnalysis of VarianceGrowth factorEndothelial CellsTransporterCoculture TechniquesElectric StimulationSignalingRatsMolneurochemistryRegional Blood FlowVibrissaeSYSNEURODigoxigeninExcitatory Amino Acid AntagonistsNeuroscience
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Anandamide-induced apoptosis in Chang liver cells involves ceramide and JNK/AP-1 pathway

2006

In the present study we demonstrate that anandamide, the most important endogenous cannabinoid, markedly induced apoptosis in Chang liver cells, an immortalized non-tumor cell line derived from normal liver tissue, while it induced only modest effects in a number of hepatoma cell lines. The apoptotic effect was reduced by methyl-beta-cyclodextrin, a membrane cholesterol depletor, suggesting an interaction between anandamide and the membrane microdomains named lipid rafts. Anandamide effects were mediated by the production of ceramide, as demonstrated by experiments performed with the sphingomyelinase inhibitor, desipramine, or with the sphingomyelinase activator, melittin. This conclusion w…

CeramideProgrammed cell deathFas Ligand ProteinCell SurvivalPolyunsaturated AlkamidesLiver cytologyp38 mitogen-activated protein kinasesBlotting WesternApoptosisArachidonic AcidsBiologyCeramidesCell LineMembrane Potentialschemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsGeneticsHumansEnzyme InhibitorsMembrane GlycoproteinsBcl-2-Like Protein 11Dose-Response Relationship DrugDesipramineJNK Mitogen-Activated Protein KinasesMembrane ProteinsFree Radical ScavengersGeneral MedicineAnandamideEndocannabinoid systemAcetylcysteineCell biologyEnzyme ActivationTranscription Factor AP-1cannabinoids apoptosis tumor cells JNK/AP1LiverchemistryApoptosisCaspasesMitochondrial MembranesTumor Necrosis FactorsApoptosis Regulatory ProteinsSphingomyelinEndocannabinoidsSignal TransductionInternational Journal of Molecular Medicine
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Changes in fatty acid compositions of total serum and lipoprotein particles, in growing rats given protein-deficient diets with either hydrogenated c…

1994

The present study examines the effects of dietary saturated (hydrogenated coconut oil) and polyunsaturated (salmon oil) fats on the composition and metabolism of lipoproteins in growing rats fed on protein-deficient diets. Four groups of rats were fed on the following diets for 28 d: 200 g casein+50 g coconut oil (COC)/kg, 20 g casein+50 g coconut oil (COd)/kg, 200 g casein + 50 g salmon oil (SAC)/kg, 20 g casein+50 g salmon oil (SAd)/kg. Both protein-deficient groups exhibited low concentrations of protein and triacylglycerol (in serum, very-low-density lipoprotein (VLDL), low-density lipoprotein-high-density lipoprotein, (LDL-HDL1) and HDL2-3), of cholesterol (in LDL-HDL1) and of phosphol…

CocosMalemedicine.medical_specialtyVery low-density lipoproteinfood.ingredientLipoproteinsMedicine (miscellaneous)Biologychemistry.chemical_compoundFish OilsfoodEssential fatty acidSalmonProtein DeficiencyInternal medicinemedicineAnimalsPlant OilsRats WistarPhospholipidsTriglycerideschemistry.chemical_classificationNutrition and DieteticsFatty AcidsCoconut oilCaseinsFatty acidBlood ProteinsFish oilDietRatsApolipoproteinsEndocrinologychemistrySaturated fatty acidCoconut Oillipids (amino acids peptides and proteins)Arachidonic acidPolyunsaturated fatty acidBritish Journal of Nutrition
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Liver X receptor activation promotes polyunsaturated fatty acid synthesis in macrophages : relevance in the context of atherosclerosis

2015

Objective— Liver X receptors (LXRs) modulate cholesterol and fatty acid homeostasis as well as inflammation. This study aims to decipher the role of LXRs in the regulation of polyunsaturated fatty acid (PUFA) synthesis in macrophages in the context of atherosclerosis. Approach and Results— Transcriptomic analysis in human monocytes and macrophages was used to identify putative LXR target genes among enzymes involved in PUFA biosynthesis. In parallel, the consequences of LXR activation or LXR invalidation on PUFA synthesis and distribution were determined. Finally, we investigated the impact of LXR activation on PUFA metabolism in vivo in apolipoprotein E–deficient mice. mRNA levels of acyl…

Context (language use)Biologydigestive systemchemistry.chemical_compoundMicearachidonic acidAnimalsHumansFatty acid homeostasisReceptorLiver X receptor[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyLiver X Receptorschemistry.chemical_classificationCholesterolFatty acidfood and beveragesArteriesAtherosclerosisOrphan Nuclear ReceptorsmacrophagesBiochemistrychemistryn-3 polyunsaturated fatty acidFatty Acids UnsaturatedArachidonic acidlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineSterol Regulatory Element Binding Protein 1Polyunsaturated fatty acidFoam Cellsliver X receptor
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