Search results for "Inflammation."

showing 10 items of 2627 documents

The anti-inflammatory and antinociceptive effects of NF-κB inhibitory guanidine derivative ME10092

2010

The guanidine compound ME10092 (1-(3,4-dimethoxy-2-chlorobenzylideneamino)-guanidine) is known to possess anti-radical and anti-ischemic activity but its molecular targets have not been identified. This study investigated whether ME10092 regulates the nuclear factor kappa B (NF-kappaB)-mediated signal transduction in vivo. The effect of ME10092 treatment (1-100 pmol/mouse) on nuclear translocation of NF-kappaB, activation of expression of inflammatory mediators and production of nitric oxide were measured in the lipopolysaccharide (LPS)-induced brain inflammation model in mice in vivo. The antinociceptive activity of ME10092 was tested in the formalin-induced paw licking test. ME10092 dose-…

LipopolysaccharidesMaleNecrosisTranscription GeneticLipopolysaccharidemedicine.drug_classInterleukin-1betaImmunologyAdministration OralNitric Oxide Synthase Type IIInflammationPharmacologyNitric OxideGuanidinesAnti-inflammatoryNitric oxideMicechemistry.chemical_compoundIn vivoFormaldehydemedicineAnimalsImmunology and AllergyPain MeasurementPharmacologyAnalgesicsMice Inbred ICRbiologyTumor Necrosis Factor-alphaAnti-Inflammatory Agents Non-SteroidalNF-kappa BNitric oxide synthasechemistryCyclooxygenase 2Immunologybiology.proteinEncephalitisInflammation Mediatorsmedicine.symptomLickingSignal TransductionInternational Immunopharmacology
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Intravitreal injection of bevacizumab induces inflammatory alterations in a uveitis experimental model.

2010

PurposeBevacizumab is currently used as an intravitreal agent in the treatment of inflammatory-associated eye diseases. The aim of the current study is to explore the effects of the intravitreal injection of bevacizumab on aqueous humour cytokines and chemokines in an experimental uveitis model.MethodsEndotoxin-induced uveitis was induced in rats by footpad injections. Bevacizumab was administered by intravitreal injection (75 μg in 3–μL samples) and different chemokine and cytokine proteins were quantified in aqueous humor.ResultsIntravitreal administration of bevacizumab led to a several-fold increase of RANTES, MCP-1, and IFN-γ concentrations in aqueous humor of endotoxin-treated rats.Co…

LipopolysaccharidesMaleVascular Endothelial Growth Factor AChemokinegenetic structuresBevacizumabmedicine.medical_treatmentInflammationAngiogenesis InhibitorsEnzyme-Linked Immunosorbent AssayPharmacologyAntibodies Monoclonal HumanizedAqueous HumorUveitisInterferon-gammaMedicineAnimalsChemokine CCL5Chemokine CCL2biologybusiness.industryAqueous humourGeneral MedicineIntravitreal administrationmedicine.diseaseeye diseasesRatsBevacizumabOphthalmologyDisease Models AnimalCytokineRats Inbred LewMonoclonalIntravitreal Injectionsbiology.proteinCytokinessense organsmedicine.symptombusinessUveitismedicine.drugEuropean journal of ophthalmology
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Beta- and gamma-melanocortins inhibit lipopolysaccharide induced nitric oxide production in mice brain.

2003

The pro-opiomelanocortin-derived peptide alpha-melanocyte stimulating hormone (alpha-MSH) mediates many diverse physiological actions, including anti-inflammatory and immunomodulatory effects. However, little is known about the physiological roles of the other melanocortins, beta- and gamma-MSH. Here, we investigated the effects of melanocortin peptides in an in vivo neuroinflammation model. Six hours following intracisternal (i.c.) administration of 10 microg lipopolysaccharide (LPS) to mice a five-fold increase in the nitric oxide (NO) level was seen in the animals' brains, when detected by electron paramagnetic resonance (EPR). All tested melanocortins, alpha-, beta-, gamma1- and gamma2-…

LipopolysaccharidesMaleendocrine systemmedicine.medical_specialtyLipopolysaccharideCentral nervous systemInflammationPharmacologyBiologyNitric OxideNitric oxidechemistry.chemical_compoundMicegamma-MSHIn vivoInternal medicinebeta-MSHmedicineAnimalsMolecular BiologyNeuroinflammationMelanocortinsFeedback PhysiologicalMice Inbred ICRintegumentary systemDose-Response Relationship DrugGeneral NeuroscienceElectron Spin Resonance SpectroscopyBrainDisease Models Animalmedicine.anatomical_structureEndocrinologychemistryalpha-MSHNeurology (clinical)Melanocortinmedicine.symptomInflammation Mediatorshormones hormone substitutes and hormone antagonistsDevelopmental BiologySignal TransductionBrain research
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Beta-MSH inhibits brain inflammation via MC(3)/(4) receptors and impaired NF-kappaB signaling.

2005

The anti-inflammatory effects of melanocortin peptides have been demonstrated in different inflammation models. This is the first report describing the molecular mechanisms for the beta-MSH-induced suppression of bacterial lipopolisaccharide (LPS)-caused brain inflammation. We found that beta-MSH suppresses LPS-induced nuclear translocation of the transcription factor NF-kappaB, and inhibits the expression of inducible nitric oxide synthase, and the following nitric oxide overproduction in the brain, in vivo. Moreover, administering the preferentially MC(4) receptor selective antagonist HS014 blocked completely these effects, suggesting a tentative MC(4) receptor mediated mechanism of actio…

LipopolysaccharidesMalemedicine.medical_specialtyImmunologyNitric Oxide Synthase Type IIInflammationElectrophoretic Mobility Shift AssayNitric OxidePeptides CyclicNitric oxidechemistry.chemical_compoundMiceInternal medicinebeta-MSHmedicineImmunology and AllergyAnimalsDrug InteractionsReceptorBrain ChemistryMice Inbred ICRbiologyDose-Response Relationship DrugImmunochemistryElectron Spin Resonance SpectroscopyNF-kappa BNF-κBHormonesCell biologyNitric oxide synthaseDisease Models AnimalEndocrinologyNeurologyMechanism of actionchemistrybiology.proteinEncephalitisReceptor Melanocortin Type 4Neurology (clinical)medicine.symptomMelanocortinSignal transductionhormones hormone substitutes and hormone antagonistsReceptor Melanocortin Type 3Signal TransductionJournal of neuroimmunology
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Hepatic over-expression of TGF-beta1 promotes LPS-induced inflammatory cytokine secretion by liver cells and endotoxemic shock.

2005

Transforming growth factor-beta (TGF-beta) is an important suppressor of inflammation. However, TGF-beta has also been found to promote secretion of inflammatory cytokines, and transgenic mice, which constitutively express TGF-beta in liver, have been found to be more susceptible to endotoxemia. To approach this apparent paradox, we investigated the role of hepatic TGF-beta1 in endotoxemia by utilising inducible TGF-beta1-transgenic mice that express TGF-beta1 under control of the C-reactive protein promoter. In contrast to non-transgenic littermates, administration of lipopolysaccharide (LPS) induced strongly increased expression of TGF-beta and acute phase proteins in the TGF-beta1-transg…

LipopolysaccharidesMalemedicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentImmunologyInflammationMice TransgenicBiologyProinflammatory cytokineTransforming Growth Factor beta1chemistry.chemical_compoundMiceImmune systemTransforming Growth Factor betaInternal medicinemedicineImmunology and AllergyAnimalsSecretionAcute-Phase ReactionCells CulturedInterleukin-6Acute-phase proteinEndotoxemiaCytokineEndocrinologychemistryHepatocytesCytokine secretionmedicine.symptomInflammation MediatorsImmunology letters
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ttCH, a selective inhibitor of inducible nitric oxide synthase expression with antiarthritic properties

2003

In a previous work, we investigated the effects of a series of dimethoxy- and trimethoxychalcone derivatives, with various patterns of fluorination, on nitric oxide production in lipopolysaccharide-stimulated murine RAW 264.7 cells. The present study was designed to determine if 2,4,6-trimethoxy-2'-trifluoromethylchalcone (ttCH) could modulate the production of nitric oxide (NO) and/or prostaglandins in vitro and in vivo. On the mouse macrophage cell line RAW 264.7, ttCH inhibited dose-dependently NO and prostaglandin E(2) production, with IC(50) in the micromolar range. This compound had no direct inhibitory effect on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 activities. …

LipopolysaccharidesMalemedicine.medical_treatmentBlotting WesternNitric Oxide Synthase Type IIPharmacologyCarrageenanNitric OxideDinoprostoneCell LineNitric oxideMicechemistry.chemical_compoundIn vivomedicineAnimalsEdemaEnzyme InhibitorsProstaglandin E2InflammationPharmacologybiologyChemistryMacrophagesAnti-Inflammatory Agents Non-SteroidalBiological activityArthritis ExperimentalHindlimbRatsCarrageenanIsoenzymesRadiographyNitric oxide synthaseMechanism of actionBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesRats Inbred Lewbiology.proteinFemaleNitric Oxide Synthasemedicine.symptomProstaglandin Emedicine.drugEuropean Journal of Pharmacology
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Ciona intestinalis peroxinectin is a novel component of the peroxidase–cyclooxygenase gene superfamily upregulated by LPS

2013

Peroxinectins function as hemoperoxidase and cell adhesion factor involved in invertebrate immune reaction. In this study, the ascidian (Ciona intestinalis) peroxinectin gene (CiPxt) and its expression during the inflammatory response have been examined. CiPxt is a new member of the peroxidase-cyclooxygenase gene superfamily that contains both the peroxidase domain and the integrin KGD (Lys-Gly-Asp) binding motif. A phylogenetic tree showed that CiPxt is very close to the chordate group and appears to be the outgroup of mammalian MPO, EPO and TPO clades. The CiPxt molecular structure model resulted superimposable to the human myeloperoxidase. The CiPxt mRNA expression is upregulated by LPS …

LipopolysaccharidesModels MolecularHemocytesLPSAmino Acid MotifsMolecular Sequence DataPeroxinectinImmunologyIntegrinSettore BIO/05 - ZoologiaChordatePeroxinectin;Peroxidase;Inflammation;LPS;Ciona intestinalisAnimalsCiona intestinalisAmino Acid SequenceRNA MessengerCell adhesionPhylogenyPeroxidaseInflammationRegulation of gene expressionSequence Homology Amino AcidbiologyCell adhesion moleculeAnimal Structuresbiology.organism_classificationMolecular biologyImmunity InnateProtein Structure TertiaryCiona intestinalisGene Expression RegulationPeroxidasesOrgan SpecificityMyeloperoxidaseembryonic structuresImmunologybiology.proteinCell Adhesion MoleculesDevelopmental BiologyEndostyleDevelopmental & Comparative Immunology
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New insight into the inhibition of the inflammatory response to experimental delayed-type hypersensitivity reactions in mice by scropolioside A.

2006

Scropolioside A, an iridoid isolated from Scrophularia auriculata ssp. pseudoauriculata, showed anti-inflammatory properties against different experimental models of delayed-type hypersensitivity. This iridoid reduced the oedema induced by oxazolone by 79% (72 h) at 0.5 mg/ear while reducing that induced by sheep red blood cells by 47% (18 h), 45% (24 h) and 36% (48 h) at 10 mg/kg. In vivo it reduced both oedema formation and cell infiltration whereas in vitro it reduced the proliferation of activated T-lymphocytes (IC50 of 67.74 microM). Treatment with scropolioside A (100 microM) 18 and 24 h after phytohemagglutinin stimulation increased the number of cells arrested in the subG(0) phase w…

LipopolysaccharidesNecrosisErythrocytesLeukotriene B4NeutrophilsT-LymphocytesAnti-Inflammatory AgentsStimulationInflammationApoptosisLymphocyte proliferationPharmacologyBiologyLeukotriene B4DinoprostoneNitric oxideCell LineOxazolonechemistry.chemical_compoundMiceGlucosidesmedicineAnimalsEdemaHumansHypersensitivity DelayedPyransPharmacologySheepPancreatic ElastaseCaspase 3MacrophagesOxazoloneEarAllergenschemistryDelayed hypersensitivityImmunologyCytokinesFemalemedicine.symptomEuropean journal of pharmacology
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A role for Toll-like receptor mediated signals in neutrophils in the pathogenesis of the anti-phospholipid syndrome.

2012

The anti-phospholipid syndrome (APS) is characterized by recurrent thrombosis and occurrence of anti-phospholipid antibodies (aPL). aPL are necessary, but not sufficient for the clinical manifestations of APS. Growing evidence suggests a role of innate immune cells, in particular polymorphonuclear neutrophils (PMN) and Toll-like receptors (TLR) to be additionally involved. aPL activate endothelial cells and monocytes through a TLR4-dependent signalling pathway. Whether this is also relevant for PMN in a similar way is currently not known. To address this issue, we used purified PMN from healthy donors and stimulated them in the presence or absence of human monoclonal aPL and the TLR4 agonis…

LipopolysaccharidesNeutrophilsImmunology610 MedizinImmunoglobulinslcsh:MedicineInflammationApoptosisImmunopathologyBiologyNeutrophil ActivationAutoimmune DiseasesPhagocytosisimmune system diseases610 Medical sciencesmedicineHumansInterleukin 8L-SelectinReceptorlcsh:ScienceBiologyImmune ResponseneoplasmsRespiratory BurstInflammationToll-like receptorMultidisciplinaryInnate immune systemCD11b AntigenCoagulation DisordersEffectorInterleukin-8lcsh:RImmunityHematologyAntiphospholipid SyndromeFlow CytometryInnate ImmunityRespiratory burstToll-Like Receptor 4ImmunologyTLR4MedicineClinical Immunologylcsh:Qmedicine.symptomResearch ArticleSignal TransductionPLoS ONE
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Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

2009

Cells of the monocyte-macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-kappaB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-kappaB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-kappaB inhibits NF-kappaB-driven, M1-polariz…

LipopolysaccharidesP50Macrophage polarizationRegulatorInflammationBiologyImmune toleranceMiceCell polaritymedicineImmune ToleranceMacrophageAnimalsHumansCells CulturedMice KnockoutMultidisciplinaryMacrophagesCell PolarityNF-kappa B p50 SubunitNF-kappa B p50 SubunitInterferon-betaBiological SciencesCell biologyEndotoxinsSTAT1 Transcription FactorImmunologymedicine.symptom
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