Search results for "NFKB"

showing 10 items of 34 documents

Shikonin reduces oedema induced by phorbol ester by interfering with IκBα degradation thus inhibiting translocation of NF-κB to the nucleus

2010

Background and purpose In the present paper we studied the effect of shikonin on ear oedema induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), and determined the mechanisms through which shikonin might exert its topical anti-inflammatory action. Experimental approach Acute ear oedema was induced in mice by topical application of TPA. The in vitro assays used macrophages RAW 264.7 cells stimulated with lipopolysaccharide. Cyclooxygenase-2, inducible nitric oxide synthase, protein kinase Calpha, extracellular signal-regulated protein kinase (ERK), phosphorylated ERK (pERK), c-Jun N-terminal kinase (JNK), pJNK, p38, p-p38, p65, p-p65, inhibitor protein of nuclear factor-kappaB (NF-kappaB) …

PharmacologyMAPK/ERK pathwayIκBαKinasep38 mitogen-activated protein kinasesMitogen-activated protein kinasebiology.proteinElectrophoretic mobility shift assayBiologyNFKB1Protein kinase AMolecular biologyBritish Journal of Pharmacology
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Role of nuclear factor-κB and heme oxygenase-1 in the mechanism of action of an anti-inflammatory chalcone derivative in RAW 264.7 cells

2004

The synthetic chalcone 3',4',5',3,4,5-hexamethoxy-chalcone (CH) is an anti-inflammatory compound able to reduce nitric oxide (NO) production by inhibition of inducible NO synthase protein synthesis. In this work, we have studied the mechanisms of action of this compound. CH (10-30 microm) prevents the overproduction of NO in RAW 264.7 macrophages stimulated with lipopolysaccharide (1 microg ml(-1)) due to the inhibition of nuclear factor kappaB (NF-kappaB) activation. We have shown that treatment of cells with CH results in diminished degradation of the NF-kappaB-IkappaB complex leading to inhibition of NF-kappaB translocation into the nucleus, DNA binding and transcriptional activity. We a…

PharmacologyOxygenaseChalconebiologyChemistryNFKB1Nitric oxideHeme oxygenaseNitric oxide synthasechemistry.chemical_compoundBiochemistryMechanism of actionmedicinebiology.proteinmedicine.symptomHemeBritish Journal of Pharmacology
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The carbon monoxide-releasing molecule CORM-2 inhibits the inflammatory response induced by cytokines in Caco-2 cells

2007

Background and purpose: Recent evidence indicates that carbon monoxide-releasing molecules (CO-RMs) exhibit potential anti-inflammatory properties. In the present study, we have investigated whether tricarbonyl dichloro ruthenium(II) dimer (CORM-2) can control the inflammatory response induced by cytokines in a human colonic epithelial cell line, Caco-2. Experimental approach: Caco-2 cells were preincubated with CORM-2 for 30 minutes and then stimulated with interleukin (IL)-1β, tumor necrosis factor-α and interferon-γ for different times. Gene expression was analyzed by real-time PCR. Protein expression was investigated by Western blot and ELISA. Transcription factor activation was determi…

PharmacologySmall interfering RNACytokinep38 mitogen-activated protein kinasesEnhancer bindingmedicine.medical_treatmentGene expressionmedicineTumor necrosis factor alphaBiologyNFKB1Protein kinase AMolecular biologyBritish Journal of Pharmacology
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Antipsoriatic effects of avarol-3′-thiosalicylate are mediated by inhibition of TNF-αgeneration and NF-κB activation in mouse skin

2007

Background and purpose: Avarol is a marine sesquiterpenoid hydroquinone with anti-inflammatory and antipsoriatic properties. The aim of this study was to evaluate the in vitro and in vivo pharmacological behaviour of the derivative avarol-3′-thiosalicylate (TA) on some inflammatory parameters related to the pathogenesis of psoriasis. Experimental approach: Human neutrophils and monocytes as well as the human keratinocyte cell line HaCaT were used to study the effect of TA on oxidative stress, the arachidonic acid pathway, tumour necrosis factor-α (TNF-α) release and nuclear factor-κB (NF-κB) activation. All these parameters were also determined in vivo using the zymosan induced mouse air po…

Pharmacologymedicine.medical_specialtyLeukotriene B4ZymosanPharmacologyBiologyNFKB1HaCaTchemistry.chemical_compoundmedicine.anatomical_structureEndocrinologyEicosanoidchemistryIn vivoInternal medicinemedicineTumor necrosis factor alphaKeratinocyteBritish Journal of Pharmacology
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Cacospongionolide B suppresses the expression of inflammatory enzymes and tumour necrosis factor-αby inhibiting nuclear factor-κB activation

2003

The marine product cacospongionolide B, a sesterterpene isolated from the Mediterranean sponge Fasciospongia cavernosa, is an inhibitor of secretory phospholipase A2 with anti-inflammatory properties. In this work, we have studied the mechanism of action of this compound in the inflammatory response induced by zymosan in primary cells and in the mouse air pouch. In mouse peritoneal macrophages, cacospongionolide B was able to downregulate the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), resulting in decreased production of NO and prostaglandin E2 (PGE2). This compound also reduced tumour necrosis factor-α (TNF-α) mRNA expression and TNF-α levels. Cacosp…

Pharmacologymedicine.medical_specialtyNecrosisbiologyZymosanNFKB1Molecular biologyNitric oxide synthasechemistry.chemical_compoundEndocrinologyMechanism of actionchemistryInternal medicinemedicinebiology.proteinTumor necrosis factor alphamedicine.symptomProstaglandin E2Transcription factormedicine.drugBritish Journal of Pharmacology
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Nuclear Translocation of Nuclear Transcription Factor-κB by α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptors Leads to Transcription of …

2003

We describe a new molecular mechanism of cell death by excitotoxicity mediated through nuclear transcription factor κB (NFκB) in rat embryonic cultures of dopaminergic neurons. Treatment of mesencephalic cultures with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) resulted in a number of changes that occurred selectively in dopaminergic neurons, including persistent elevation in intracellular Ca2+ monitored with Fura-2, and a significant increase in intramitochondrial oxidation of dihydrorhodamine 123, probably associated with transient increase of mitochondrial permeability, cytochrome c release, nuclear translocation of NFκB, and transcriptional activation of the oncogenep53.…

Programmed cell deathCell Membrane PermeabilityTime FactorsCIENCIAS MÉDICAS Y DE LA SALUDTranscription GeneticNeuriteActive Transport Cell NucleusInmunologíaExcitotoxicitymedicine.disease_causeCELL DEATHReceptors DopamineRats Sprague-DawleymedicineAnimalsReceptors AMPAalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidTranscription factorPARKINSON DISEASECaspaseNeuronsPharmacologyCell DeathNUCLEAR TRANSCRIPTIONbiologyDopaminergicNF-kappa BNFKB1Molecular biologyMitochondriaRatsCell biologyMedicina Básicabiology.proteinMolecular MedicineCalciumFemaleTumor Suppressor Protein p53Signal transductionMolecular Pharmacology
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Production of reactive oxygen intermediates by human macrophages exposed to soot particles and asbestos fibers and increase in NF-kappa B p50/p105 mR…

1999

Alveolar macrophages (AM) play a decisive role in the immunologic defense system of the lung and in inflammatory pulmonary pathomechanisms. AM and blood monocytes (BM) were exposed to chrysotile B, soot FR 101, and Printex 90 (P 90). We evaluated the reactive oxygen intermediate (ROI) release of AM and BM after particle exposure. ROI release was measured by chemiluminescence. Thirty-minute exposure caused a significant (up to 2.5-fold) increase in ROI release of AM (100 micrograms/10(6) cells) compared with control experiments (p0.01). Identical exposure conditions for BM resulted in a similar reaction pattern (maximum 2.2-fold increase in ROI release; p0.05). After a 90-min particle exposu…

Pulmonary and Respiratory MedicineAdultMaleP50Asbestos Serpentinemedicine.medical_treatmentMonocytesProinflammatory cytokineSuperoxide dismutaseGene expressionMacrophages AlveolarmedicineHumansRNA MessengerReceptorCells CulturedAgedLungbiologyDose-Response Relationship DrugChemistryReverse Transcriptase Polymerase Chain ReactionNF-kappa BMiddle AgedNFKB1Molecular biologyCarbonCytokinemedicine.anatomical_structureGene Expression RegulationImmunologyLuminescent Measurementsbiology.proteinFemaleReactive Oxygen SpeciesBronchoalveolar Lavage FluidLung
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Les IAP au cœur de la signalisation NF-κB

2012

The function of IAP has long been limited to an inhibition of apoptosis through their capacity to bind some caspases. Since the expression of these proteins is altered in some tumor samples, IAPs are targets for anticancer therapy and many small molecules have been designed for their capacity to inhibit IAP-caspase interaction. Unexpectedly, these molecules appeared to significantly affect NF-κB activation. In this review, we will discuss the central role of cIAP1, cIAP2 and XIAP in the regulation of NF-κB activating signaling pathways.

Regulation of gene expressionbiologyGeneral MedicineTransforming growth factor betaNFKB1General Biochemistry Genetics and Molecular BiologyCell biologyXIAPbody regionsApoptosisImmunologybiology.proteinSignal transductionReceptorCaspasemédecine/sciences
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MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
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Changes associated with aging and replicative senescence in the regulation of transcription factor nuclear factor-kappa B.

1996

Both the aging of animals and the senescence of cultured cells involve an altered pattern of gene expression, suggesting changes in transcription factor regulation. We studied age-related changes in transcription factors nuclear factor (NF)-kappa B, activator protein factor-1 (AP-1) and Sp-1 by using electrophoretic mobility shift binding assays; we also analysed changes in the protein components of NF-kappa B complex with Western blot assays. Nuclear and cytoplasmic extracts were prepared from heart, liver, kidney and brain of young adult and old NMRI mice and Wistar rats as well as from presenescent, senescent and simian virus 40-immortalized human WI-38 fibroblasts. Aging of both mice an…

SenescenceMaleAgingBlotting WesternSimian virus 40BiologyTransfectionBiochemistryCell LineMiceWestern blotGene expressionmedicineAnimalsHumansRats WistarMolecular BiologyTranscription factorLungCellular SenescenceCell Line TransformedRegulation of gene expressionReporter genemedicine.diagnostic_testMyocardiumNF-kappa BGene Expression Regulation DevelopmentalHeartCell BiologyNFKB1Molecular biologyRecombinant ProteinsRatsB vitaminsLiverFemaleCell DivisionResearch Article
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