Search results for "arachidonic acid"

showing 10 items of 178 documents

Interaction of antibodies to proteinase 3 (classic anti-neutrophil cytoplasmic antibody) with human renal tubular epithelial cells: impact on signali…

2002

Abstract Among the anti-neutrophil cytoplasmic Abs (ANCA), those targeting proteinase 3 (PR3) have a high sensitivity and specificity for Wegener’s granulomatosis (WG). A pathogenetic role for these autoantibodies has been proposed due to their capacity of activating neutrophils in vitro. Recently, PR3 was also detected in human renal tubular epithelial cells (TEC). In the present study, the effect of murine monoclonal anti-PR3 Abs (anti-PR3) and purified c-ANCA targeting PR3 from WG serum on isolated human renal tubular cell signaling and inflammatory mediator release was characterized. Priming of TEC with TNF-α resulted in surface expression of PR3, as quantified in immunofluorescence stu…

Intracellular Fluidmedicine.medical_specialtyMyeloblastinImmunologyImmunofluorescencePhosphatidylinositolsAutoantigensDinoprostoneFlow cytometryAntibodies Antineutrophil CytoplasmicAntigen-Antibody ReactionsThromboxane A2Proteinase 3SuperoxidesInternal medicinemedicineCyclic AMPImmunology and AllergyHumanscardiovascular diseasesCells CulturedArachidonic Acidmedicine.diagnostic_testbiologyHydrolysisImmune SeraCell MembraneSerine EndopeptidasesAntibodies MonoclonalEpithelial CellsLipid signalingIn vitroCell biologyEndocrinologyKidney Tubulesbiology.proteinCyclooxygenaseSignal transductionInflammation MediatorsIntracellularSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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Release of choline in the isolated heart, an indicator of ischemic phospholipid degradation and its protection by ischemic preconditioning: No eviden…

2003

Abstract The release of choline as a water-soluble product of phospholipid hydrolysis was measured in the perfusate of rat hearts to monitor ischemic membrane degradation and its protection by ischemic preconditioning (IPC). Hearts were subjected to global ischemia (GI; 30 min of no-flow) followed by 60 min of reperfusion. To induce IPC, GI was preceded by four no-flow episodes of 5 min each. Deleterious consequences of GI and reperfusion, namely coronary flow reduction, incidence of arrhythmias and release of cardiac troponin T, were significantly attenuated by IPC. The release of choline increased during reperfusion in a biphasic manner: a first phase peaked immediately after GI and was f…

IschemiaPhospholipid610 Medicine & healthArachidonic AcidsPharmacologyPhospholipasePhospholipases AGeneral Biochemistry Genetics and Molecular Biology3000 General Pharmacology Toxicology and PharmaceuticsCholineRats Sprague-Dawleychemistry.chemical_compoundTroponin T1300 General Biochemistry Genetics and Molecular Biologyparasitic diseasesPhospholipase DmedicineAnimalsCholinecardiovascular diseasesGeneral Pharmacology Toxicology and PharmaceuticsPhospholipidsPhospholipase APhospholipase DMyocardiumGeneral Medicinemedicine.diseaseRatsPhospholipases A2CytosolchemistryBiochemistry10054 Clinic for Psychiatry Psychotherapy and PsychosomaticsIschemic Preconditioning MyocardialIschemic preconditioninghuman activities
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A study of the novel anti-inflammatory agent florifenine topical anti-inflammatory activity and influence on arachidonic acid metabolism and neutroph…

1995

We have evaluated the effects of the novel anti-inflammatory agent florifenine, 2-(1-Pyrrolidinyl)ethyl N-[7-(trifluoromethyl)-4-quinolyl]anthranilate, on topical inflammation in mice, free radical-mediated reactions, arachidonic acid metabolism and some neutrophil functions. Topical administration of florifenine produced dose-related anti-inflammatory activity in 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced ear oedema and with a lower potency, in the response induced by arachidonic acid (AA). Florifenine also inhibited neutrophil migration and PGE2 content in the inflammed ears. In human whole blood, florifenine was a potent and selective inhibitor of TXB2 generation. This anti-infla…

Leukocyte migrationPyrrolidinesCell SurvivalNeutrophilsmedicine.drug_classAdministration TopicalAnti-Inflammatory AgentsInflammationIn Vitro TechniquesPharmacologyAntioxidantsAnti-inflammatoryMicechemistry.chemical_compoundSuperoxidesmedicineAnimalsEdemaHumansPancreatic elastasePharmacologyArachidonic AcidPancreatic ElastaseHydroxyl RadicalChemistrySuperoxideAnti-Inflammatory Agents Non-SteroidalElastaseZymosanFree Radical ScavengersGeneral MedicineRatsImmunologyAminoquinolinesEicosanoidsTetradecanoylphorbol AcetateArachidonic acidLipid Peroxidationmedicine.symptomLeukocyte ElastaseNaunyn-Schmiedeberg's Archives of Pharmacology
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Effects of nordihydroguaiaretic acid on murine antibody-dependent cellular cytotoxicity.

1996

The purpose of this study was to analyze the effects of nordihydroguaiaretic acid, an inhibitor of the lipoxygenase pathway of arachidonic acid, on antibody-dependent cellular cytotoxicity. Antibody-dependent cellular cytotoxicity mediated by murine spleen cells was significantly inhibited by concentrations of nordihydroguaiaretic acid from 10(-5) to 10(-4) M (1C50 = 2 x 10(-5) M). The inhibitory effect of nordihydroguaiaretic acid was also observed on antibody-dependent cellular cytotoxicity mediated by macrophage-depleted spleen cells as well as isolated macrophages. Nordihydroguaiaretic acid was highly effective when added at the beginning of the assay and was always present throughout t…

Leukotriene B4Clinical BiochemistrySpleenIn Vitro TechniquesLeukotriene B4chemistry.chemical_compoundLipoxygenaseMicemedicineAnimalsMasoprocolLipoxygenase InhibitorsCytotoxicityAntibody-dependent cell-mediated cytotoxicityMice Inbred BALB CbiologyMacrophagesAntibody-Dependent Cell CytotoxicityNordihydroguaiaretic acidKineticsmedicine.anatomical_structurechemistryBiochemistryEnzyme inhibitorbiology.proteinArachidonic acidSpleenInternational journal of clinicallaboratory research
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Endogenous nitric oxide inhibits leukotriene B4 release from rat alveolar macrophages

1997

Effects of endogenous nitric oxide (NO) on the release of mediators of the lipoxygenase and cyclo-oxygenase pathway from rat alveolar macrophages were studied. Alveolar macrophages, freshly isolated or after 18-h culture, were incubated in (amino acid-free) Krebs medium and labelled with [3H]arachidonic acid. The release of [3H]leukotriene B4 and [3H]prostanoids (separated by high performance liquid chromatography) was determined. A 23187 was used as stimulus, as rising intracellular Ca2+ activates directly the phospholipase A2 and lipoxygenase pathway. A 23187 (10 microM) enhanced [3H]leukotriene B4 release from freshly prepared alveolar macrophages about 65-fold, but only 5- to 6-fold fro…

Leukotriene B4LipoxygenaseArachidonic AcidsBiologyNitric OxideLeukotriene B4Nitric oxideRats Sprague-Dawleychemistry.chemical_compoundLipoxygenasePhospholipase A2Macrophages AlveolarmedicineAnimalsEnzyme InhibitorsCalcimycinCells CulturedChromatography High Pressure LiquidPharmacologyomega-N-MethylarginineProstanoidMolecular biologyRatsmedicine.anatomical_structurechemistryBiochemistryProstaglandin-Endoperoxide SynthasesAlveolar macrophagebiology.proteinFemaleArachidonic acidNitric Oxide SynthasePulmonary alveolusEuropean Journal of Pharmacology
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Staphylococcal alpha-toxin provokes neutrophil-dependent cardiac dysfunction: role of ICAM-1 and cys-leukotrienes.

2002

The role of polymorphonuclear neutrophils (PMN) in septic myocardial dysfunction is presently unknown. Staphylococcus aureus infections are frequently associated with septic sequelae. Therefore, we perfused isolated rat hearts with low doses of α-toxin, the major staphylococcal exotoxin, followed by application of human PMN, N-formyl-methionyl-leucyl-phenylalanine, and arachidonic acid. In contrast to sham-perfused hearts (no α-toxin), a rise in coronary perfusion pressure (CPP) and a reduction of contractile function were noted, and cardiac expression of intercellular adhesion molecule (ICAM)-1 was detected by immunohistochemical methods and real-time PCR. Histological analysis and myelope…

LeukotrienesHeart diseasePhysiologyNeutrophilsNeutrophileBacterial ToxinsExotoxinsThiophenesIn Vitro Techniquesmedicine.disease_causePathogenesisHemolysin ProteinsPhysiology (medical)medicineAnimalsHumansICAM-1Arachidonic AcidToxinbusiness.industryMyocardiumHydrazonesHeartmedicine.diseaseIntercellular Adhesion Molecule-1RatsN-Formylmethionine Leucyl-PhenylalaninePerfusionStaphylococcus aureusImmunologyCirculatory systemCardiology and Cardiovascular MedicinebusinessOligonucleotide ProbesExotoxinAmerican journal of physiology. Heart and circulatory physiology
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Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide …

2014

Macrophages come across active prostaglandin (PG) metabolism during inflammation, shunting early production of pro-inflammatory towards anti-inflammatory mediators terminating the process. This work for the first time provides evidence that a phytochemical may modulate the arachidonate (AA) metabolism in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages, promoting the ultimate formation of anti-inflammatory cyclopentenone 15deoxy-PGJ2. Added 1 h before LPS, indicaxanthin from Opuntia Ficus Indica prevented activation of nuclear factor-κB (NF-κB) and over-expression of PGE2 synthase-1 (mPGES-1), but up-regulated cyclo-oxygenase-2 (COX-2) and PGD2 synthase (H-PGDS), with final product…

LipopolysaccharidesLipid PeroxidesLipopolysaccharidePyridinesPhytochemicalsClinical BiochemistryProstaglandinIndicaxanthinmedicine.disease_causeBiochemistryCell LineMiceStructure-Activity Relationshipchemistry.chemical_compoundmedicineAnimalslcsh:QH301-705.5Inflammationlcsh:R5-920Arachidonic AcidNADPH oxidaseDose-Response Relationship DrugLipid peroxidebiologyMacrophagesOrganic ChemistryOpuntiaMetabolismOxidantsPro-oxidantBetaxanthinslcsh:Biology (General)chemistryBiochemistryOxidative stressFruitIndicaxanthin Phytochemicals Eicosanoids Inflammation Oxidative stress.Prostaglandinsbiology.proteinEicosanoidslipids (amino acids peptides and proteins)lcsh:Medicine (General)IndicaxanthinOxidative stressResearch PaperRedox Biology
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Subventricular zone neural progenitors protect striatal neurons from glutamatergic excitotoxicity.

2012

The functional significance of adult neural stem and progenitor cells in hippocampal-dependent learning and memory has been well documented. Although adult neural stem and progenitor cells in the subventricular zone are known to migrate to, maintain and reorganize the olfactory bulb, it is less clear whether they are functionally required for other processes. Using a conditional transgenic mouse model, selective ablation of adult neural stem and progenitor cells in the subventricular zone induced a dramatic increase in morbidity and mortality of central nervous system disorders characterized by excitotoxicity-induced cell death accompanied by reactive inflammation, such as 4-aminopyridine-i…

LipopolysaccharidesPolyunsaturated AlkamidesSubventricular zoneGlutamic AcidMice TransgenicArachidonic AcidsBiologyAmidohydrolasesGlutamatergicMiceNeural Stem CellsLateral VentriclesmedicineAnimalsDronabinolProgenitor cell4-Aminopyridineneurogenesis; ischaemia; neural stem cells; excitotoxicity; endocannabinoidsGanciclovirEpilepsyStem CellsNeurogenesisExcitatory Postsynaptic PotentialsNeural stem cellCorpus StriatumNeuroepithelial cellMice Inbred C57BLStrokeneurogenesisDisease Models Animalmedicine.anatomical_structureNeuroprotective AgentsBenzamidesSettore MED/26 - NeurologiaNeurology (clinical)ischaemiaCarbamatesStem cellNeuroscienceexcitotoxicityExcitatory Amino Acid AntagonistsAdult stem cellEndocannabinoidsBrain : a journal of neurology
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Effect of indomethacin on the kinetics of tumour necrosis factor alpha release and tumour necrosis factor alpha gene expression by human blood monocy…

1991

Summary In this investigation we have examined the effects of indomethacin, an inhibitor of the cyclooxygenase pathway of arachidonic acid, upon the kinetics of the release of tumour necrosis factor alpha (TNF) and of the expression of TNF gene by lipopolysaccharide (LPS)-stimulated human blood monocytes (BM). Following stimulation of BM with LPS, TNF was released within 2 h, reached peak values at 8 h and declined at subsequent time-points (24 and 48 h). Indomethacin (10−5 m ) slightly stimulated the production of TNF at 2, 4, and 8 h and prevented the decline of TNF observed at 24 and 48 h. This effect was related to the persistence of TNF synthesis, as demonstrated by kinetics evaluation…

LipopolysaccharidesTranscription GeneticLipopolysaccharideNeutrophilsmedicine.medical_treatmentIndomethacinProstaglandinIn Vitro TechniquesPharmacologyDinoprostoneCyclooxygenase pathwaychemistry.chemical_compoundGene expressionmedicineHumansRNA MessengerPharmacologyTumor Necrosis Factor-alphabusiness.industryMonocyteKineticsmedicine.anatomical_structureCytokineGene Expression RegulationchemistryImmunologyIndicators and ReagentsArachidonic acidTumor necrosis factor alphabusinessPharmacological Research
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Anandamide inhibits IL-12p40 production by acting on the promoter repressor element GA-12: Possible involvement of the COX-2 metabolite prostamide E 2

2007

The eCB [endoCB (cannabinoid)] system is being considered as a novel therapeutic target for immune disorders. Cytokines of the IL-12 (interleukin-12) family have essential functions in cell-mediated immunity. In the present study, we have addressed the mechanisms of action of the eCB AEA (anandamide) on the regulation of IL-12p40 in activated microglia/macrophages. We demonstrated that AEA can inhibit the expression of p35, p19 and p40 subunits, which form the biologically-active cytokines IL-12 and IL-23 in microglia stimulated with LPS (lipopolysaccharide)/IFNγ (interferon γ). Additionally, we have provided evidence that AEA reduces the transcriptional activity of the IL-12p40 gene in LPS…

Lipopolysaccharidesmedicine.medical_specialtyPolyunsaturated Alkamidesmedicine.medical_treatmentMolecular Sequence DataRepressorArachidonic AcidsBiologyInterleukin-23BiochemistryDinoprostoneInterferon-gammaMicechemistry.chemical_compoundInternal medicinemedicineAnimalsEthanolamidePromoter Regions GeneticReceptors CannabinoidMolecular BiologyCells CulturedRegulation of gene expressionMice Inbred BALB CInterleukin-12 Subunit p40Cell BiologyAnandamideEndocannabinoid systemCell biologyProtein SubunitsEndocrinologyGene Expression RegulationchemistryCyclooxygenase 2lipids (amino acids peptides and proteins)MicrogliaCannabinoidSignal transductionEndocannabinoidsSignal TransductionProstaglandin E
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