Search results for "NF-"

showing 10 items of 461 documents

Trans- but not cis-resveratrol impairs angiotensin-II-mediated vascular inflammation through inhibition of NF-κB activation and peroxisome proliferat…

2010

Abstract Angiotensin II (Ang-II) displays inflammatory activity and is implicated in several cardiovascular disorders. This study evaluates the effect of cis- and trans (t)-resveratrol (RESV) in two in vivo models of vascular inflammation and identifies the cardioprotective mechanisms that underlie them. In vivo, Ang-II–induced arteriolar leukocyte adhesion was inhibited by 71% by t-RESV (2.1 mg/kg, i.v.), but was not affected by cis-RESV. Because estrogens influence the rennin-angiotensin system, chronic treatment with t-RESV (15 mg/kg/day, orally) inhibited ovariectomy-induced arteriolar leukocyte adhesion by 81%, partly through a reduction of cell adhesion molecule (CAM) expression and c…

MaleChemokineEndotheliumOvariectomyImmunologyInflammationAngiogenesis InhibitorsCell CommunicationPharmacologyRats Sprague-DawleyDownregulation and upregulationStilbenesmedicineImmunology and AllergyAnimalsHumansCells CulturedbiologyCell adhesion moleculeMonocyteAngiotensin IINF-kappa BStereoisomerismAngiotensin IIRatsUp-RegulationPPAR gammaDisease Models Animalmedicine.anatomical_structureCardiovascular DiseasesResveratrolImmunologybiology.proteinFemaleEndothelium Vascularmedicine.symptomSignal transductionInflammation MediatorsJournal of immunology (Baltimore, Md. : 1950)
researchProduct

High mobility group box 1 potentiates the pro-inflammatory effects of interleukin-1β in osteoarthritic synoviocytes

2010

Introduction High mobility group box 1 (HMGB1) is released by necrotic cells or secreted in response to inflammatory stimuli. Extracellular HMGB1 may act as a pro-inflammatory cytokine in rheumatoid arthritis. We have recently reported that HMGB1 is released by osteoarthritic synoviocytes after activation with interleukin-1beta (IL-1β) The present study investigated the role of HMGB1 in synovial inflammation in osteoarthritis (OA). Methods HMGB1 was determined in human synovium using immunohistochemistry, comparing normal to OA. OA synoviocytes were incubated with HMGB1 at 15 or 25 ng/ml in the absence or presence of IL-1β (10 ng/ml). Gene expression was analyzed by quantitative PCR and pro…

MaleChemokineMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaImmunologyInflammationchemical and pharmacologic phenomenaCCL2HMGB1p38 Mitogen-Activated Protein KinasesRheumatologySynovitisMatrix Metalloproteinase 13HumansMedicineImmunology and AllergyRNA MessengerHMGB1 ProteinExtracellular Signal-Regulated MAP KinasesCells CulturedAgedbiologybusiness.industrySynovial MembraneNF-kappa BOsteoarthritis Kneemedicine.diseaseImmunohistochemistryMolecular biologyCCL20Cytokinemedicine.anatomical_structurebiology.proteinFemaleMatrix Metalloproteinase 3Matrix Metalloproteinase 1Synovial membranemedicine.symptombusinessProto-Oncogene Proteins c-aktResearch ArticleArthritis Research & Therapy
researchProduct

Hepatoprotective and anti-inflammatory effects of total flavonoids of Qu Zhi Ke (peel of Citrus changshan-huyou) on non-alcoholic fatty liver disease…

2019

Abstract Background Citrus flavonoids, consisting of naringin, narirutin, neohesperidine, etc., have therapeutic activities for the treatment of lipometabolic disorders. The peel of Citrus changshan-huyou (Qu Zhi Ke, QZK) is a new source of flavonoids, but attracted little attention so far. Hypothesis QZK should possess therapeutic effects against lipometabolic disorders due to the flavonoids it contains. Study design In this study, we extracted and purified the flavonoids of QZK (TFCH) and established an obesity-induced non-alcoholic fatty liver disease (NAFLD) model of rats. TFCH was given orally for 8 weeks, and its anti-NAFLD effects and potential mechanism were evaluated. Methods The f…

MaleCitrusmedicine.drug_classFlavonoidPharmaceutical SciencePharmacologyDiet High-FatProtective AgentsAnti-inflammatoryProinflammatory cytokineRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotNon-alcoholic Fatty Liver DiseaseDrug DiscoveryNonalcoholic fatty liver diseasemedicineAnimalsPhosphorylationNaringin030304 developmental biologyFlavonoidsPharmacologychemistry.chemical_classification0303 health sciencesNarirutinmedicine.diagnostic_testPlant ExtractsAnti-Inflammatory Agents Non-SteroidalFatty liverNF-kappa Bfood and beveragesmedicine.diseaseGene Expression RegulationLiverComplementary and alternative medicinechemistry030220 oncology & carcinogenesisMolecular MedicineMitogen-Activated Protein KinasesPhytomedicine
researchProduct

Ablation of the Regulatory IE1 Protein of Murine Cytomegalovirus Alters In Vivo Pro-inflammatory TNF-alpha Production during Acute Infection

2012

Little is known about the role of viral genes in modulating host cytokine responses. Here we report a new functional role of the viral encoded IE1 protein of the murine cytomegalovirus in sculpting the inflammatory response in an acute infection. In time course experiments of infected primary macrophages (MΦs) measuring cytokine production levels, genetic ablation of the immediate-early 1 (ie1) gene results in a significant increase in TNFα production. Intracellular staining for cytokine production and viral early gene expression shows that TNFα production is highly associated with the productively infected MΦ population of cells. The ie1- dependent phenotype of enhanced MΦ TNFα production …

MaleCytomegalovirus InfectionMuromegalovirusViral Diseasesmedicine.medical_treatmentvirusesTNF TNF-alpha murine cytomegalovirus MCMV IEVirus ReplicationMice0302 clinical medicineGene expressionBiology (General)Mice Inbred BALB C0303 health scienceseducation.field_of_studyPhysicsvirus diseasesHerpesviridae InfectionsTransfection3. Good healthGenètica microbianaInterleukin 10PhenotypeInfectious DiseasesCytokineLiverCytokinesMedicineFemaleTumor necrosis factor alphaBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.Microbial geneticsSignal TransductionResearch ArticleDNA ReplicationGene Expression Regulation ViralQH301-705.5ImmunologyPopulationBiologyMicrobiologyCell LineImmediate-Early ProteinsViral Proteins03 medical and health sciencesIn vivoVirologyGeneticsmedicineAnimalseducationMolecular Biology030304 developmental biologyTumor Necrosis Factor-alphaMacrophagesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.FísicaRC581-607Mice Inbred C57BLViral replicationDNA ViralImmunologyParasitologyImmunologic diseases. Allergy030215 immunology
researchProduct

Mild Aerobic Exercise Training Hardly Affects the Diaphragm of mdx Mice

2016

In the mdx mice model of Duchenne Muscular Dystrophy (DMD), mild endurance exercise training positively affected limb skeletal muscles, whereas few and controversial data exist on the effects of training on the diaphragm. The diaphragm was examined in mdx (C57BL/10ScSn-Dmdmdx) and wild-type (WT, C57BL/10ScSc) mice under sedentary conditions (mdx-SD, WT-SD) and during mild exercise training (mdx-EX, WT-EX). At baseline, and after 30 and 45 days (training: 5 d/wk for 6 weeks), diaphragm muscle morphology and Cx39 protein were assessed. In addition, tissue levels of the chaperonins Hsp60 and Hsp70 and the p65 subunit of nuclear factor-kB (NF-kB) were measured in diaphragm, gastrocnemius, and q…

MaleDuchenne muscular dystrophychaperoninTime FactorsDiaphragmSettore MED/10 - Malattie Dell'Apparato RespiratorioSettore BIO/09 - FisiologiaConnexinsMitochondrial ProteinsNecrosisendurance trainingAnimalsGenetic Predisposition to DiseaseHSP70 Heat-Shock Proteinsstress markersMuscle StrengthNF-kBSettore BIO/16 - Anatomia UmanaTranscription Factor RelAChaperonin 60Settore CHIM/06 - Chimica OrganicaExercise TherapyMuscular Dystrophy DuchenneDisease Models AnimalPhenotypeMice Inbred mdxPhysical Endurance
researchProduct

Clinical and Biological Heterogeneity in Children with Moderate Asthma

2003

To evaluate the relationship between inflammatory markers and severity of asthma in children, the amount of interleukin-8 (IL-8) and granulocyte/macrophage colony-stimulating factor (GM-CSF) released by peripheral blood mononuclear cells, exhaled nitric oxide (FE NO) levels, p65 nuclear factor-kappaB subunit, and phosphorylated IkBalpha expression by peripheral blood mononuclear cells were assessed in six control subjects, 12 steroid-naives subjects with intermittent asthma, and 17 children with moderate asthma. To investigate their predictive value, biomarker levels were correlated with the number of exacerbations during a 18-month follow-up period. We found that GM-CSF release was higher …

MaleExacerbationAnti-Inflammatory AgentsCritical Care and Intensive Care MedicineSynaptotagminsMedicineChildSalmeterol XinafoateCalcium-Binding ProteinMembrane GlycoproteinsRespiratory diseaseNF-kappa Binflammatory markersBronchodilator AgentsAnti-Inflammatory AgentSynaptotagmin IBiomarker (medicine)FemaleMembrane GlycoproteinAndrostadienes; Anti-Inflammatory Agents; NF-kappa B; Leukocytes Mononuclear; Membrane Glycoproteins; Granulocyte-Macrophage Colony-Stimulating Factor; Humans; Synaptotagmins; Albuterol; Asthma; Child; Receptors Cell Surface; Nerve Tissue Proteins; Nitric Oxide; Synaptotagmin I; Calcium-Binding Proteins; Interleukin-8; Adolescent; Bronchodilator Agents; Male; Biological Markers; Femalemedicine.symptomHumanmedicine.drugPulmonary and Respiratory MedicineAdolescentNerve Tissue ProteinsReceptors Cell SurfaceInflammationNitric OxidePeripheral blood mononuclear cellFluticasone propionateHumansAlbuterolBronchodilator AgentAsthmaAndrostadienefluticasone propionatebusiness.industryCalcium-Binding ProteinsInterleukin-8Granulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseSynaptotagminAsthmaAndrostadienesasthma; inflammatory markers; fluticasone propionateNerve Tissue ProteinBiological MarkerExhaled nitric oxideImmunologyLeukocytes MononuclearFluticasonebusinessBiomarkersAmerican Journal of Respiratory and Critical Care Medicine
researchProduct

A protein quality control pathway regulated by linear ubiquitination.

2019

Neurodegenerative diseases are characterized by the accumulation of misfolded proteins in the brain. Insights into protein quality control mechanisms to prevent neuronal dysfunction and cell death are crucial in developing causal therapies. Here, we report that various disease-associated protein aggregates are modified by the linear ubiquitin chain assembly complex (LUBAC). HOIP, the catalytic component of LUBAC, is recruited to misfolded Huntingtin in a p97/VCP-dependent manner, resulting in the assembly of linear polyubiquitin. As a consequence, the interactive surface of misfolded Huntingtin species is shielded from unwanted interactions, for example with the low complexity sequence doma…

MaleHuntingtinSp1 protein humanProtein aggregationHTT protein humanDeubiquitinating enzymegenetics [Huntington Disease]Micegenetics [Sp1 Transcription Factor]0302 clinical medicineUbiquitinpathology [Brain]Valosin Containing Proteincytology [Fibroblasts]pathology [Neurons]PolyubiquitinCells CulturedMice Knockout0303 health sciencesHuntingtin ProteinGeneral NeuroscienceNF-kappa Bgenetics [Huntingtin Protein]Middle AgedCell biologymetabolism [Polyubiquitin]pathology [Huntington Disease]metabolism [Neurons]metabolism [NF-kappa B]Protein foldingFemalemetabolism [Fibroblasts]Protein BindingSignal TransductionAdultmetabolism [Valosin Containing Protein]Sp1 Transcription Factorcytology [Embryo Mammalian]genetics [Valosin Containing Protein]BiologyGeneral Biochemistry Genetics and Molecular Biologymetabolism [Sp1 Transcription Factor]03 medical and health sciencesddc:570Gene silencingAnimalsHumansmetabolism [Huntington Disease]Protein Interaction Domains and MotifsMolecular Biologymetabolism [Embryo Mammalian]030304 developmental biologyAgedSp1 transcription factorGeneral Immunology and MicrobiologyUbiquitinationProteotoxicitymetabolism [Brain]Case-Control Studiesmetabolism [Huntingtin Protein]biology.proteinProtein Processing Post-Translational030217 neurology & neurosurgerygenetics [NF-kappa B]
researchProduct

In vitro anticholinergic drugs affect CD8+ peripheral blood T-cells apoptosis in COPD

2011

Novel pharmacological strategies are aimed at the resolution of systemic inflammation in COPD potentiating peripheral blood T-cell (PBT-cell) apoptosis. Although muscarinic acetylcholine receptors (mAChRs) M(3) and choline-acetyltransferase (ChAT) participate in the airway inflammation of COPD, their role in PBT-cell apoptosis remains unexplained. We evaluated in PBT-cells from COPD patients, smoker (S) and control (C) subjects: (1) apoptosis (by annexin V binding), (2) mAChR M(3) and ChAT expression, acetylcholine (ACh)-binding; (3) choline levels in serum and PBT-cells extracts. We tested the effects of Tiotropium (Spiriva(®)) and hemicholinium-3 (HCh-3) on apoptosis, NFκB pathway, caspas…

MaleImmunologyScopolamine DerivativesApoptosisCD8-Positive T-LymphocytesPharmacologySystemic inflammationCholinergic AntagonistsCholineCholine O-AcetyltransferasePulmonary Disease Chronic ObstructiveAnnexinMuscarinic acetylcholine receptormedicineHumansImmunology and AllergyLymphocyte CountTiotropium BromideCaspaseAgedReceptor Muscarinic M3Caspase 8COPDbiologyCaspase 3Systemic inflammation Non-neuronal components of cholinergic system Caspases NF B pathwaybusiness.industryNF-kappa BHematologyTiotropium bromideMiddle Agedmedicine.diseaserespiratory tract diseasesEnzyme ActivationApoptosisbiology.proteinFemalemedicine.symptombusinessAcetylcholineProtein BindingSignal Transductionmedicine.drugImmunobiology
researchProduct

Mitochondrial biogenesis fails in secondary biliary cirrhosis in rats leading to mitochondrial DNA depletion and deletions

2011

Chronic cholestasis is characterizedby mitochondrial dysfunction, associated with loss of mitochondrialmembrane potential, decreased activities of respiratory chaincomplexes, and ATP production. Our aim was to determine themolecular mechanisms that link long-term cholestasis to mitochondrialdysfunction. We studied a model of chronic cholestasis inducedby bile duct ligation in rats. Key sensors and regulators of theenergetic state and mitochondrial biogenesis, mitochondrial DNA(mtDNA)-to-nuclear DNA (nDNA) ratio (mtDNA/nDNA) relativecopy number, mtDNA deletions, and indexes of apoptosis (BAX,BCL-2, and cleaved caspase 3) and cell proliferation (PCNA) wereevaluated. Our results show that long…

MaleMitochondrial DNAPhysiologyMitochondrial TurnoverMitochondrial HepatopathyNF-E2-Related Factor 1Respiratory chainMitochondria LiverProtein Serine-Threonine KinasesMitochondrionBiologyDNA MitochondrialSirtuin 1CholestasisProliferating Cell Nuclear AntigenPhysiology (medical)medicineAnimalsRats Wistarbcl-2-Associated X ProteinCholestasisHepatologyCaspase 3Liver Cirrhosis BiliaryGastroenterologyPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA-Binding ProteinsTFAMmedicine.diseaseGA-Binding Protein Transcription FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyRatsGenes MitochondrialProto-Oncogene Proteins c-bcl-2Mitochondrial biogenesisChronic DiseaseBile DuctsGene DeletionTranscription FactorsAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
researchProduct

Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
researchProduct