Search results for "inflammatory cytokine"

showing 10 items of 464 documents

Silibinin improves hepatic and myocardial injury in mice with nonalcoholic steatohepatitis

2012

Abstract Background Nonalcoholic fatty liver disease is a chronic metabolic disorder with significant impact on cardiovascular and liver mortality. Aims In this study, we examined the effects of silibinin on liver and myocardium injury in an experimental model of nonalcoholic fatty liver disease. Methods A four-week daily dose of silibinin (20 mg/kg i.p.) was administrated to db/db mice fed a methionine–choline deficient diet. Hepatic and myocardial histology, oxidative stress and inflammatory cytokines were evaluated. Results Silibinin administration decreased HOMA-IR, serum ALT and markedly improved hepatic and myocardial damage. Silibinin reduced isoprostanes, 8-deoxyguanosine and nitrit…

MaleGene ExpressionIsoprostanesmedicine.disease_causeGastroenterologyAntioxidantsMicechemistry.chemical_compoundMethionineNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseasePhosphorylationGastroenterologyAlanine TransaminaseGlutathioneCholine DeficiencyMitochondrial respiratory chainLiverHeart Inflammation NAFLD Oxidative stress SilibininCytokinesmedicine.symptomSilymarinmedicine.medical_specialtySilibininInflammationStatistics NonparametricProinflammatory cytokineInsulin resistanceInternal medicinemedicineAnimalsNitritesAnalysis of VarianceNitratesHepatologySettore BIO/16 - Anatomia Umanabusiness.industryMyocardiumJNK Mitogen-Activated Protein KinasesGlutathionemedicine.diseaseDietFatty LiverOxidative StressEndocrinologychemistrySilybinInsulin ResistancebusinessOxidative stressDigestive and Liver Disease
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Molecular adaptations of the blood–brain barrier promote stress resilience vs. depression

2020

Significance Thirty to fifty percent of depressed individuals are unresponsive to commonly prescribed antidepressant treatments, suggesting that biological mechanisms, such as stress-induced inflammation and blood vessel dysfunction, remain untreated. The blood–brain barrier is the ultimate frontier between the brain and harmful toxins or inflammatory signals circulating in the blood. Depression and vulnerability to chronic social stress are associated with loss of this barrier integrity; however, the mechanisms involved remain poorly understood. Identification of adaptations leading to resilience under stressful conditions could help develop novel treatments. Here we combined behavioral, p…

MaleHistone Deacetylase 1InflammationFOXO1Blood–brain barrierNucleus AccumbensEpigenesis GeneticProinflammatory cytokineMice03 medical and health sciences0302 clinical medicinevascularmedicineAnimalsHumansClaudin-5030304 developmental biologyInflammationSocial stressDepressive Disorder Major0303 health sciencesantidepressantMultidisciplinaryDepressionbusiness.industrySystems BiologyBiological Sciencesmedicine.diseasemood disordersAntidepressive Agents3. Good healthMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureMood disordersBlood-Brain BarrierMajor depressive disorderAntidepressantmedicine.symptombusinessNeuroscienceStress Psychologicalepigenetic030217 neurology & neurosurgerySignal TransductionProceedings of the National Academy of Sciences
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Anti-inflammatory and antioxidant effects of muscarinic acetylcholine receptor (mAChR) activation in the rat hippocampus

2019

AbstractRecently we found that acute treatment with Oxotremorine (Oxo), a non-selective mAChRs agonist, up-regulates heat shock proteins and activates their transcription factor heat shock factor 1 in the rat hippocampus. Here we aimed to investigate: a) if acute treatment with Oxo may regulate pro-inflammatory or anti-inflammatory cytokines and oxidative stress in the rat hippocampus; b) if chronic restraint stress (CRS) induces inflammatory or oxidative alterations in the hippocampus and whether such alterations may be affected by chronic treatment with Oxo. In the acute experiment, rats were injected with single dose of Oxo (0.4 mg/kg) and sacrificed at 24 h, 48 h and 72 h. In the CRS ex…

MaleHydrocortisonemedicine.medical_treatmentInterleukin-1betaNeuroimmunologyAnti-Inflammatory Agentslcsh:MedicinePharmacologymedicine.disease_causeHippocampusSettore BIO/09 - FisiologiaAntioxidantsSuperoxide Dismutase-1Muscarinic acetylcholine receptorPhosphorylationlcsh:Sciencechemistry.chemical_classificationMultidisciplinarybiologyneurodegenerationAlzheimer's diseaseReceptors MuscarinicNeuroprotective AgentsCytokineSignal Transductionmedicine.drugRestraint PhysicalAgonistmedicine.drug_classScopolaminemuscarinic acetylcholine receptorMuscarinic AgonistsArticleOxotremorine anti-inflammatory cytokinesSuperoxide dismutaseHeat shock proteinOxotremorinemedicineAnimalsRats WistarInflammationReactive oxygen speciesInterleukin-6Superoxide DismutaseOxotremorinelcsh:RTranscription Factor RelARatsOxidative Stresschemistrybiology.proteinlcsh:QReactive Oxygen SpeciesProtein Processing Post-TranslationalOxidative stressScientific Reports
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Complement C1q is dramatically up-regulated in brain microglia in response to transient global cerebral ischemia.

2000

Abstract Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marke…

MaleImmunologyIschemiaInflammationIn situ hybridizationBiologySulfur RadioisotopesProinflammatory cytokineRNA ComplementaryCerebrospinal fluidDownregulation and upregulationmedicineImmunology and AllergyAnimalsTransient (computer programming)Rats WistarComplement C1qIn Situ HybridizationPharmacologyMicrogliaComplement C1qBrainRNA Probesmedicine.diseaseImmunohistochemistryCell biologyComplement systemRatsUp-Regulationmedicine.anatomical_structureIschemic Attack TransientImmunologyMicrogliamedicine.symptomNeuroscienceDigoxigeninJournal of immunology (Baltimore, Md. : 1950)
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The Carbon Monoxide-Releasing Molecule Tricarbonyldichlororuthenium(II) Dimer Protects Human Osteoarthritic Chondrocytes and Cartilage from the Catab…

2008

We have investigated the effects of a carbon monoxide-releasing molecule, tricarbonyldichlororuthenium(II) dimer (CORM-2), on catabolic processes in human osteoarthritis (OA) cartilage and chondrocytes activated with interleukin-1beta. In these cells, proinflammatory cytokines induce the synthesis of matrix metalloproteinases (MMPs) and aggrecanases, including members of a disintegrin and metalloproteinase with thrombospondin domain (ADAMTS) family, which may contribute to cartilage loss. CORM-2 down-regulated MMP-1, MMP-3, MMP-10, MMP-13, and ADAMTS-5 in OA chondrocytes, and it inhibited cartilage degradation. These effects were accompanied by increased aggrecan synthesis and collagen II e…

MaleInterleukin-1betaDown-RegulationMatrix metalloproteinaseProtective AgentsProinflammatory cytokineExtracellular matrixChondrocytesOsteoarthritisOrganometallic CompoundsmedicineExtracellularHumansAggrecansCollagen Type IIAggrecanAgedPharmacologyCarbon MonoxideThrombospondinChemistryCartilageADAMTSMatrix MetalloproteinasesCell biologyCartilagemedicine.anatomical_structureBiochemistryMolecular MedicineFemaleJournal of Pharmacology and Experimental Therapeutics
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HLA and killer cell immunoglobulin-like receptor (KIRs) genotyping in patients with acute ischemic stroke

2019

Abstract Introduction In humans, a major component of natural killer (NK) and T cell target recognition depends on the surveillance of human leukocyte antigen (HLA) class I molecules by killer immunoglobulin-like receptors (KIRs). Aims To implement the knowledge about the immunological genetic background of acute ischemic stroke susceptibility in relation to the frequency of the KIR genes and HLA alleles. Methods Subjects with acute ischemic stroke and subjects without stroke were genotyped for the presence of KIR genes and of the three major KIR ligand groups, HLA-C1, HLA-C2, and HLA-Bw4, both HLA-B and HLA-A loci. Results Between November 2013 and February 2016, consecutive patients with …

MaleKiller immunoglobulin-like receptors (KIRs)0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaNeurologyGenotypeT cellKIR LigandImmunologyKiller-cell immunoglobulin-like receptorchemical and pharmacologic phenomenaHuman leukocyte antigenlcsh:RC346-429Proinflammatory cytokine03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineReceptors KIRotorhinolaryngologic diseasesHumansMedicineGenetic Predisposition to DiseaseReceptorStrokelcsh:Neurology. Diseases of the nervous systemAgedSettore MED/04 - Patologia GeneraleNeuroscience (all)business.industryResearchGeneral NeuroscienceHistocompatibility Antigens Class IMiddle Agedmedicine.diseaseStrokeHLACross-Sectional Studies030104 developmental biologymedicine.anatomical_structureNeurologyImmunologyFemalebusiness030217 neurology & neurosurgeryJournal of Neuroinflammation
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Inflammation-Induced Alteration of Astrocyte Mitochondrial Dynamics Requires Autophagy for Mitochondrial Network Maintenance

2013

Accumulating evidence suggests that changes in the metabolic signature of astrocytes underlie their response to neuroinflammation, but how proinflammatory stimuli induce these changes is poorly understood. By monitoring astrocytes following acute cortical injury, we identified a differential and region-specific remodeling of their mitochondrial network: while astrocytes within the penumbra of the lesion undergo mitochondrial elongation, those located in the core-the area invaded by proinflammatory cells-experience transient mitochondrial fragmentation. In brain slices, proinflammatory stimuli reproduced localized changes in mitochondrial dynamics, favoring fission over fusion. This effect w…

MaleLipopolysaccharidesPhysiologyDnm1l protein mouseInterleukin-1betaNitric Oxide Synthase Type IIMitochondrionAstrocytes/metabolismMitochondrial DynamicsAutophagy-Related Protein 7Mice0302 clinical medicinemetabolism [Reactive Oxygen Species]PhosphorylationCells Culturedcytology [Astrocytes]0303 health sciencesmetabolism [Inflammation]metabolism [Astrocytes]Inflammation/metabolismCytokines/metabolismdrug effects [Mitochondria]Mitochondria/drug effectsMitochondriaCell biologyAstrocytes/drug effectsmedicine.anatomical_structureMicrotubule-Associated Proteins/metabolismPhosphorylationCytokinesmetabolism [Dynamins]Nitric Oxide Synthase Type II/metabolismMicrotubule-Associated ProteinsAstrocytegenetics [Microtubule-Associated Proteins]DynaminsProgrammed cell deathAstrocytes/cytologydrug effects [Astrocytes]Mice TransgenicBiologypharmacology [Interferon-gamma]Proinflammatory cytokine03 medical and health sciencesInterferon-gammametabolism [Interleukin-1beta]reactive astrocytesReactive Oxygen Species/metabolismddc:570Mitochondria/metabolismtoxicity [Lipopolysaccharides]medicineAutophagyAnimalsAutophagy-Related Protein 7Molecular BiologyNeuroinflammation030304 developmental biologypathology [Inflammation]Dynamins/metabolismInflammationdrug effects [Mitochondrial Dynamics]Autophagymetabolism [Cytokines]Interferon-gamma/pharmacologyCell Biologymetabolism [Microtubule-Associated Proteins]Microtubule-Associated Proteins/geneticsMitochondrial Dynamics/drug effectsmetabolism [Mitochondria]metabolism [Nitric Oxide Synthase Type II]Mice Inbred C57BLLipopolysaccharides/toxicityAtg7 protein mouseAstrocytesInterleukin-1beta/metabolismReactive Oxygen Species030217 neurology & neurosurgeryInflammation/pathologyCell Metabolism
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Pentoxifylline Prevents Loss of PP2A Phosphatase Activity and Recruitment of Histone Acetyltransferases to Proinflammatory Genes in Acute Pancreatitis

2009

Mitogen-activated protein kinases (MAPKs) are considered major signal transducers early during the development of acute pancreatitis. Pentoxifylline is a phosphodiesterase inhibitor with marked anti-inflammatory properties through blockade of extracellular signal regulated kinase (ERK) phosphorylation and tumor necrosis factor alpha production. Our aim was to elucidate the mechanism of action of pentoxifylline as an anti-inflammatory agent in acute pancreatitis. Necrotizing pancreatitis induced by taurocholate in rats and taurocholate-treated AR42J acinar cells were studied. Phosphorylation of ERK and ERK kinase (MEK1/2), as well as PP2A, PP2B, and PP2C serine/threonine phosphatase activiti…

MaleMAPK/ERK pathwayChromatin ImmunoprecipitationPhosphodiesterase InhibitorsBlotting WesternPhosphataseAnti-Inflammatory AgentsPharmacologyBiologyCell LinePentoxifyllineProinflammatory cytokineCyclic AMPPhosphoprotein PhosphatasesmedicineAnimalsPentoxifyllineRats WistarExtracellular Signal-Regulated MAP KinasesHistone AcetyltransferasesInflammationPharmacologyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaProtein phosphatase 2medicine.diseaseCyclic Nucleotide Phosphodiesterases Type 2RatsEnzyme ActivationPancreatitisBiochemistryAcute DiseaseRNAMolecular MedicinePhosphorylationPancreatitisMitogen-Activated Protein KinasesChromatin immunoprecipitationmedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Autoimmune skin inflammation is dependent on plasmacytoid dendritic cell activation by nucleic acids via TLR7 and TLR9

2010

Lupus-prone mice develop a chronic inflammatory response to cutaneous injury that depends on the production of type I interferon, TLR7, and TLR9.

MaleMice 129 StrainImmunologyGene ExpressionInflammationchemical and pharmacologic phenomenaMice Inbred StrainsReceptor Interferon alpha-betaBiologySkin DiseasesArticleProinflammatory cytokinePathogenesisTLR9MiceAutoimmune skin inflammationimmune system diseasesNucleic AcidsmedicineImmunology and AllergyAnimalsLupus Erythematosus SystemicReceptorskin and connective tissue diseasesTLR7SkinAutoimmune skin inflammation; TLR7; TLR9; plasmacytoid dendritic cells.Mice KnockoutPlasmacytoid dendritic cell activationLupus erythematosusReverse Transcriptase Polymerase Chain ReactionTLR9virus diseaseshemic and immune systemsTLR7DNADendritic Cellsmedicine.diseaseFlow CytometryMice Inbred C57BLplasmacytoid dendritic cells.Toll-Like Receptor 7Toll-Like Receptor 9ImmunologyMyeloid Differentiation Factor 88CytokinesFemalemedicine.symptomThe Journal of Experimental Medicine
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MyD88 is dispensable for resistance toParacoccidioides brasiliensisin a murine model of blood-borne disseminated infection

2008

We have studied the role of MyD88, an adaptor protein of Toll-like receptors (TLRs), in murine defenses against Paracoccidioides brasiliensis in a model of blood-borne disseminated infection. Wild-type (WT) and MyD88-deficient mice infected intravenously with P. brasiliensis yeast cells showed an equivalent fungal burden, as well as similar levels of proinflammatory IL-1beta, IL-6, IL-12p70, tumor necrosis factor (TNF)-alpha and MIP-2, T-helper type 1 (Th1) (IFN-gamma) and Th2 cytokines (IL-4) in tissue homogenates. In vitro production of TNF-alpha, IFN-gamma and IL-12p70, by antigen-stimulated splenocytes from infected animals, was also similar in both types of mice; this production of Th1…

MaleMicrobiology (medical)medicine.medical_treatmentImmunologyNerve Tissue ProteinsMicrobiologyParacoccidioidesMicrobiologyProinflammatory cytokineMicePeritoneal cavitymedicineAnimalsHumansImmunology and AllergyLectins C-TypeMice KnockoutParacoccidioides brasiliensisbiologyMembrane ProteinsParacoccidioidesGeneral MedicineTh1 Cellsbiology.organism_classificationToll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4Disease Models AnimalTLR2Infectious Diseasesmedicine.anatomical_structureCytokineMyeloid Differentiation Factor 88Macrophages PeritonealTLR4CytokinesTumor necrosis factor alphaParacoccidioidomycosisFungemiaFEMS Immunology & Medical Microbiology
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