Search results for "Type I"

showing 10 items of 966 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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Responses of retinal arterioles and ciliary arteries in pigs with acute respiratory distress syndrome (ARDS)

2019

Abstract Acute respiratory distress syndrome (ARDS) is a clinical syndrome of acute lung failure in critically sick patients, which severely compromises the function of multiple organs, including the brain. Although, the optic nerve and the retina are a part of the central nervous system, the effects of ARDS on these ocular structures are completely unknown. Thus, the major goal of this study was to test the hypothesis that ARDS affects vascular function in the eye. ARDS was induced in anesthetized pigs by intratracheal injection of lipopolysaccharide (LPS). Sham-treated animals served as controls. Pigs were monitored for 8 h and then sacrificed. Subsequently, retinal arterioles and short p…

LipopolysaccharidesMalePathologymedicine.medical_specialtyARDSEndotheliumRetinal ArterySwineNitric Oxide Synthase Type IIEnzyme-Linked Immunosorbent AssayVasodilationReal-Time Polymerase Chain ReactionCiliary ArteriesCellular and Molecular Neurosciencechemistry.chemical_compoundGlutathione Peroxidase GPX1medicine.arterymedicineAnimalsRNA MessengerEndothelial dysfunctionGlutathione PeroxidaseRespiratory Distress SyndromeRetinaMicroscopy Videobusiness.industryInterleukinsRetinalShort posterior ciliary arteriesCatalasemedicine.diseaseSensory SystemsCiliary arteriesArteriolesDisease Models AnimalOphthalmologymedicine.anatomical_structurechemistryEndothelium VascularHypoxia-Inducible Factor 1Reactive Oxygen SpeciesbusinessExperimental Eye Research
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Highly efficient liposome-mediated gene transfer of inducible nitric oxide synthase in vivo and in vitro in vascular smooth muscle cells.

2000

Objective: The efficient introduction of regulatory genes into vascular smooth muscle cells (SMCs) is one of the most promising options for gene therapy of cardiovascular diseases. Cationic liposome-mediated gene transfer may become a favorable transfection technique with regard to patient’s safety for in vivo administration. However, this method until now has its limitation in a low transfection efficiency. Therefore, the present study was designed to improve cationic liposome-mediated transfection of rabbit vascular SMCs in vitro and in vivo, in order to enhance transfection efficiency and present an optimized system which may offer a potential therapeutic benefit for in vivo application.…

LipopolysaccharidesMalePathologymedicine.medical_specialtyVascular smooth musclePhysiologyTransgeneGenetic enhancementBlotting WesternGenetic VectorsGene ExpressionNitric Oxide Synthase Type IIApoptosisCoronary DiseaseBiologyMuscle Smooth VascularIn vivoPhysiology (medical)Culture TechniquesmedicineCell AdhesionAnimalsHumansRegulator geneReporter geneReverse Transcriptase Polymerase Chain ReactionGenetic transferGene Transfer TechniquesTransfectionGenetic TherapyFlow CytometryCell biologyRabbitsNitric Oxide SynthaseCardiology and Cardiovascular MedicineCell DivisionCardiovascular 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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Transcriptional up-regulation of nNOS in the dorsal vagal complex during low endotoxemia

2005

The present study analyses the expression and distribution of neuronal nitric oxide synthase (nNOS) in the brainstem of animals pre-treated with Escherichia coli or Helicobacter pylori LPS, at doses that modulate gastric motor function. Systemic administration of H. pylori LPS prevented in a dose-dependent manner (5, 40 and 100 microg kg(-1), i.v.) the increase in intragastric pressure induced by 2-deoxy-D-glucose (200 mg kg(-1), i.v.) in urethane-anaesthetized rats. Quantitative analysis showed a significant increase in the amount of nNOS mRNA induced by E. coli or H. pylori LPS (2 h later), in a segment of the brainstem containing the dorsal vagal complex (DVC). Immunohistochemical studie…

LipopolysaccharidesMalemedicine.medical_specialtyNerve Tissue ProteinsNitric Oxide Synthase Type Imedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyRats Sprague-DawleyDownregulation and upregulationInternal medicineEscherichia coliPressuremedicineAnimalsGeneral Pharmacology Toxicology and PharmaceuticsEscherichia coliMessenger RNAbiologyStomachVagus NerveGeneral MedicineHelicobacter pyloribiology.organism_classificationEndotoxemiaRatsUp-RegulationEndocrinologyDorsal motor nucleusAnesthesiaSystemic administrationImmunohistochemistryBrainstemNitric Oxide SynthaseBrain StemLife Sciences
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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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Interaction of dicaffeoylquinic derivatives with peroxynitrite and other reactive nitrogen species.

2008

Plant phenolic antioxidants, among them catechins and hydroxycinnamoyl conjugates, constitute a well defined class of inhibitors of reactive nitrogen species (RNS). To gain deeper insight in this field, we examined the effects of 3,5-di-O-caffeoylquinic acid (DCA), its methyl ester (DCE) and epigallocatechin gallate (EGCG) in nitrative and oxidative processes. These compounds were found to be strong inhibitors of the nitration of tyrosine residues induced by ONOO- in bovine seroalbumin, with their IC50 values (10-40 microM) notably decreasing in the presence of bicarbonate. When studied on the intracellular protein tyrosine nitration induced by ONOO- in cultured murine fibroblasts as well a…

LipopolysaccharidesNeutrophilsBicarbonateBiophysicsQuinic AcidNitric Oxide Synthase Type IIEpigallocatechin gallateBiochemistryCatechinNitric oxidechemistry.chemical_compoundInhibitory Concentration 50MiceNitrationPeroxynitrous AcidAnimalsHumansTyrosineMolecular BiologyReactive nitrogen speciesNitritesNitratesNitrotyrosineMacrophagesSerum Albumin BovineFibroblastsReactive Nitrogen SpeciesStimulation ChemicalBicarbonateschemistryBiochemistryTetradecanoylphorbol AcetateTyrosineCattleOxidation-ReductionPeroxynitriteArchives of biochemistry and biophysics
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Colocalization but differential regulation of neuronal NO synthase and nicotinic acetylcholine receptor in C2C12 myotubes.

2003

In mammalian skeletal muscle, neuronal-type nitric oxide synthase (nNOS) is found to be enriched at neuromuscular endplates. Here we demonstrate the colocalization of the nicotinic acetylcholine receptor (nAChR, stained with α-bungarotoxin) and nNOS (stained with a specific antibody) in murine C2C12myotubes. However, coimmunoprecipitation experiments demonstrated no evidence for a direct protein-protein association between the nAChR and nNOS in C2C12myotubes. An antibody to the α1-subunit of the nAChR did not coprecipitate nNOS, and an nNOS-specific antibody did not precipitate the α1-subunit of the nAChR. Treatment of mice with bacterial LPS downregulated the expression of nNOS in skeletal…

LipopolysaccharidesPhysiologyMuscle Fibers SkeletalNitric Oxide Synthase Type IReceptors NicotinicCell LineInterferon-gammaMicemedicineAnimalsProtein IsoformsTissue DistributionRNA MessengerMuscle SkeletalMice Inbred C3HbiologyMyogenesisSkeletal muscleColocalizationCell BiologyMolecular biologyNitric oxide synthaseNicotinic acetylcholine receptormedicine.anatomical_structureNicotinic agonistnervous systembiology.proteinNitric Oxide SynthaseC2C12Acetylcholinemedicine.drugAmerican journal of physiology. Cell physiology
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Protection by nitric oxide against liver inflammatory injury in animals carrying a nitric oxide synthase-2 transgene

2001

22 pages, 7 figures, 1 table.

Lipopolysaccharidesmedicine.medical_specialtyLipopolysaccharideTransgeneBlotting WesternNitric Oxide Synthase Type IIApoptosisGalactosamineMice TransgenicLipopolysaccharideNitric OxideBiochemistryLiver cellsProinflammatory cytokineNitric oxidechemistry.chemical_compoundMiceInternal medicineGeneticsmedicineAnimalsTransgenesPromoter Regions GeneticMolecular BiologyLiver injurybiologyTumor Necrosis Factor-alphaNF-kappa BNitric oxide synthase 2medicine.diseaseEndotoxinsEndocrinologychemistryLiverbiology.proteinTumor necrosis factor alphaNitric Oxide SynthasePhosphoenolpyruvate carboxykinaseFood DeprivationBiotechnologyInterleukin-1
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Dominant negative MORT1/FADD rescues mice from CD95 and TNF-induced liver failure

2002

Derangement of the apoptotic program is considered an important cause of liver disease. It became clear that receptor-mediated apoptosis is of specific interest in this context, and CD95 and CD120a, both members of the tumor necrosis factor (TNF) receptor superfamily, are the most prominent cell death receptors involved. The death signal is induced upon ligand binding by recruitment of caspases via the adapter molecule MORT1/FADD to the receptor and their subsequent activation. To investigate the role of MORT1/FADD in hepatocyte apoptosis, we generated transgenic mice expressing liver-specific dominant negative mutant. Mice looked grossly normal; breeding and liver development were not diff…

Lipopolysaccharidesmedicine.medical_specialtyProgrammed cell deathFas-Associated Death Domain ProteinOligonucleotidesMice TransgenicAntibodiesReceptors Tumor Necrosis FactorMiceLiver diseaseAntigens CDAlbuminsInternal medicinemedicineAnimalsfas ReceptorFADDPromoter Regions GeneticAdaptor Proteins Signal TransducingLiver injuryHepatitisMice Inbred BALB CHepatologybiologyTumor Necrosis Factor-alphamedicine.diseaseFas receptorMice Inbred C57BLEndocrinologyReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinTumor necrosis factor alphaCarrier ProteinsLiver FailureHepatology
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