Search results for "NF-"

showing 10 items of 461 documents

Xanthine oxidase-induced oxidative stress causes activation of NF-κB and inflammation in the liver of type I diabetic rats

2009

We previously showed that xanthine oxidase activity increases in type I diabetic animals and that this is a significant cause of the oxidative stress which occurs in the disease. The aim of this work was to search for molecular links between xanthine oxidase-induced oxidative stress and inflammation in Type I diabetes and to assess the ability of allopurinol, a drug widely used in clinical practice, to prevent both processes. 3-month-old male Wistar rats were made diabetic by injection (i.p.) of either streptozotocin or alloxan. Allopurinol (32 mg/Kg) was administered (i.p) to diabetic rats after they had shown clear signs of diabetes such as glucosuria and polyuria. Hepatic phospho-IKKbeta…

MaleTranscriptional ActivationXanthine Oxidasemedicine.medical_specialtyNeutrophilsAllopurinolAllopurinolInterleukin 6Free radicalsInflammationmedicine.disease_causeBiochemistryStreptozocinDiabetes Mellitus ExperimentalDiabetic complicationsProinflammatory cytokineInterleukin 1βchemistry.chemical_compoundCell MovementPhysiology (medical)Internal medicineDiabetes mellitusAlloxanmedicineAnimalsRats WistarXanthine oxidasePolyuriabusiness.industryAllopurinol; Interleukin 1β; Interleukin 6; Diabetic complications; Free radicalsNF-kappa BXanthineStreptozotocinmedicine.diseaseRatsOxidative StressEndocrinologyLiverchemistryCytokinesInflammation Mediatorsmedicine.symptombusinessOxidative stressmedicine.drugFree Radical Biology and Medicine
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Vitamin E deficiency induces liver nuclear factor-κB DNA-binding activity and changes in related genes

2005

The biological functions of vitamin E have been classically attributed to its property as a potent inhibitor of lipid peroxidation in cellular membranes. However, in 1991, Azzi's group first described that alpha-tocopherol inhibits smooth muscle cell proliferation in a protein kinase C (PKC)-dependent way, demonstrating a non-antioxidant cell signalling function for vitamin E. More recently, the capacity of alpha-tocopherol to modulate gene expression with the implication of different transcription factors, beyond its antioxidant properties, has also been established. This study was to determine the effect of vitamin E-deficiency on liver nuclear factor-kappa B (NF-kappaB) DNA-binding activ…

MaleVitaminChromatin ImmunoprecipitationGlutamate-Cysteine Ligasemedicine.medical_treatmentBlotting WesternBiologyBiochemistrychemistry.chemical_compoundCyclin D1CyclinsMalondialdehydemedicineAnimalsVitamin EVitamin E DeficiencyRNA MessengerRats WistarTranscription factorVitamin EBody WeightNF-kappa BPromoterDNAGeneral MedicineCell cycleGlutathioneRatsCell biologyGene Expression RegulationLiverBiochemistrychemistryVitamin E deficiencyChromatin immunoprecipitationFree Radical Research
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Metformin increases APP expression and processing via oxidative stress, mitochondrial dysfunction and NF-κB activation: Use of insulin to attenuate m…

2015

AbstractClinical and experimental biomedical studies have shown Type 2 diabetes mellitus (T2DM) to be a risk factor for the development of Alzheimer's disease (AD). This study demonstrates the effect of metformin, a therapeutic biguanide administered for T2DM therapy, on β-amyloid precursor protein (APP) metabolism in in vitro, ex vivo and in vivo models. Furthermore, the protective role of insulin against metformin is also demonstrated. In LAN5 neuroblastoma cells, metformin increases APP and presenilin levels, proteins involved in AD. Overexpression of APP and presenilin 1 (Pres 1) increases APP cleavage and intracellular accumulation of β-amyloid peptide (Aβ), which, in turn, promotes ag…

Maleendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causeAntioxidantsNF-κBAmyloid beta-Protein PrecursorAspartic Acid EndopeptidasesInsulinBiguanideNF-kappa BBrainAlzheimer's diseaseMetforminMetforminMitochondriaProtein TransportAntioxidantmedicine.drugmetformin T2DM Alzheimer's diseaseAdultmedicine.medical_specialtyProgrammed cell deathmedicine.drug_classOxidative phosphorylationBiologyAntidiabetic drugModels BiologicalPresenilinInternal medicineCell Line Tumormental disordersmedicinePresenilin-1AnimalsHumansMolecular BiologyCell NucleusSettore MED/04 - Patologia GeneraleAmyloid beta-PeptidesInsulinAdenylate KinaseOxidative Stress Pathwaynutritional and metabolic diseasesCell BiologyHydrogen PeroxideMice Inbred C57BLEndocrinologyGene Expression RegulationCytoprotectionOxidative stressLeukocytes MononuclearAmyloid Precursor Protein SecretasesOxidative stressBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Molecular mechanisms of hepatotoxic cholestasis by clavulanic acid: Role of NRF2 and FXR pathways.

2021

Treatment of β-lactamase positive bacterial infections with a combination of amoxicillin (AMOX) and clavulanic acid (CLAV) causes idiosyncratic drug-induced liver injury (iDILI) in a relevant number of patients, often with features of intrahepatic cholestasis. This study aims to determine serum bile acid (BA) levels in amoxicillin/clavulanate (A + C)-iDILI patients and to investigate the mechanism of cholestasis by A + C in human in vitro hepatic models. In six A + C-iDILI patients, significant elevations of serum primary conjugated BA definitely demonstrated A + C-induced cholestasis. In cultured human Upcyte hepatocytes and HepG2 cells, CLAV was more cytotoxic than AMOX, and, at subcytoto…

Malemedicine.drug_classNF-E2-Related Factor 2Receptors Cytoplasmic and NuclearCholestasis IntrahepaticPharmacologyToxicologyCholesterol 7 alpha-hydroxylaseCell Linechemistry.chemical_compoundDownregulation and upregulationCholestasismedicineHumansClavulanic AcidAgedLiver injuryBile acidChemistryGeneral MedicineGlutathioneMiddle Agedmedicine.diseaseFarnesoid X receptorFemaleCYP8B1Food ScienceSignal TransductionFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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Direct evidence of leukocyte adhesion in arterioles by angiotensin II

2004

AbstractAlthough leukocytes adhere in arteries in various vascular diseases, to date no endogenous proinflammatory molecule has been identified to initiate leukocyte adhesion in the arterial vasculature. This study was undertaken to assess angiotensin II (Ang II)-induced leukocyte adhesion in arterioles in vivo. Rats received intraperitoneal injections of Ang II; 4 hours later, leukocyte recruitment in mesenteric microcirculation was examined using intravital microscopy. Ang II (1 nM) produced significant arteriolar leukocyte adhesion of mononuclear cells. Using function-blocking monoclonal antibodies (mAbs) against different rat cell adhesion molecules (CAMs), we discovered that this effec…

Malemedicine.medical_specialtyEndotheliumIntegrin alpha4ImmunologyIntercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1BiologyBiochemistryRats Sprague-DawleyVenulesInternal medicineCell AdhesionLeukocytesmedicineAnimalsVasoconstrictor AgentsLeukocyte RollingCell adhesionCell adhesion moleculeAngiotensin IINF-kappa BCell BiologyHematologyIntercellular Adhesion Molecule-1Angiotensin IIRatsArteriolesmedicine.anatomical_structureEndocrinologyCD18 AntigensImmunologyEndothelium VascularIntravital microscopySelectinArteryBlood
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Impaired Vitamin D Signaling in Endothelial Cell Leads to an Enhanced Leukocyte-Endothelium Interplay: Implications for Atherosclerosis Development

2015

Endothelial cell activation leading to leukocyte recruitment and adhesion plays an essential role in the initiation and progression of atherosclerosis. Vitamin D has cardioprotective actions, while its deficiency is a risk factor for the progression of cardiovascular damage. Our aim was to assess the role of basal levels of vitamin D receptor (VDR) on the early leukocyte recruitment and related endothelial cell-adhesion-molecule expression, as essential prerequisites for the onset of atherosclerosis. Knockdown of VDR in endothelial cells (shVDR) led to endothelial cell activation, characterized by upregulation of VCAM-1, ICAM-1 and IL-6, decreased peripheral blood mononuclear cell (PBMC) ro…

Malemedicine.medical_specialtyEndotheliumMedicinalcsh:MedicineDown-RegulationVascular Cell Adhesion Molecule-1InflammationCell CommunicationBiologyCalcitriol receptorCell LineEndothelial activationMiceEndothelial cellNF-KappaB Inhibitor alphaInternal medicineCell AdhesionmedicineAnimalsHumansMacrophageEndotheliumVitamin Dlcsh:ScienceCell adhesionMultidisciplinaryInterleukin-6lcsh:RNF-kappa BEndothelial CellsAtherosclerosisIntercellular Adhesion Molecule-1Plaque AtheroscleroticUp-RegulationMice Inbred C57BLEndothelial stem cellIκBαmedicine.anatomical_structureEndocrinologyLeukocytes MononuclearReceptors Calcitriollcsh:QFemaleI-kappa B Proteinslipids (amino acids peptides and proteins)medicine.symptomSignal TransductionResearch ArticlePLOS ONE
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Circulating TNF-alpha and its soluble receptors during experimental acute pancreatitis.

2004

Clinical and experimental studies have shown increased concentrations of TNF-α and its soluble receptors in serum of patients with acute pancreatitis. In this work, we have investigated the time-course of TNF-α and its soluble receptors during taurocholate-induced acute pancreatitis. In addition, since TNF-α itself could mediate the shedding of its receptors, we have assessed the effect of inhibiting TNF-α production on the release of soluble TNF-α receptors in experimental acute pancreatitis. Our results indicate that soluble receptors are released in the early stages of the disease and this increase is concomitant with the release of TNF-α, which is mainly bound to specific proteins. The …

Malemedicine.medical_specialtyImmunologyInflammationBiochemistryDNA-binding proteinReceptors Tumor Necrosis FactorPentoxifyllineInternal medicinemedicineSIRSImmunology and AllergyAnimalsPentoxifyllineRats WistarReceptorMolecular BiologyInflammationbusiness.industryTumor Necrosis Factor-alphaHematologymedicine.diseasesTNF-αRRatsDisease Models AnimalEndocrinologyPancreatitisSolubilityTNF-αAcute DiseasePancreatitisAcute pancreatitisTumor necrosis factor alphamedicine.symptombusinessmedicine.drugCytokine
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Silibinin modulates lipid homeostasis and inhibits nuclear factor kappa B activation in experimental nonalcoholic steatohepatitis.

2012

Nonalcoholic steatohepatitis (NASH) is associated with increased liver-related mortality. Disturbances in hepatic lipid homeostasis trigger oxidative stress and inflammation (ie, lipotoxicity), leading to the progression of NASH. This study aimed at identifying whether silibinin may influence the molecular events of lipotoxicity in a mouse model of NASH. Eight-week-old db/db mice were fed a methionine-choline deficient (MCD) diet for 4 weeks and treated daily with silibinin (20 mg/kg intraperitoneally) or vehicle. Liver expression and enzyme activity of stearoyl-CoA desaturase-1 and acyl-CoA oxidase, and expression of liver fatty acid-binding protein were assessed. Hepatic levels of reactiv…

Malemedicine.medical_specialtyMice ObeseSilibininmedicine.disease_causeAntioxidantsTranslational Research BiomedicalMicechemistry.chemical_compoundMethionineNon-alcoholic Fatty Liver DiseasePhysiology (medical)Internal medicineNonalcoholic fatty liver diseasemedicineTBARSAnimalsHomeostasisNASH MCD Silibinin lipotoxicity.Reactive nitrogen speciesLiver injurychemistry.chemical_classificationReactive oxygen speciesAnti-Inflammatory Agents Non-SteroidalBiochemistry (medical)NF-kappa BPublic Health Environmental and Occupational HealthGeneral MedicineLipid Metabolismmedicine.diseaseCholine DeficiencyFatty LiverDisease Models AnimalOxidative StressEndocrinologyLiverchemistryLipotoxicitySilybinOxidative stressSilymarin
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The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
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Neuroimmune and Mu-Opioid Receptor Alterations in the Mesocorticolimbic System in a Sex-Dependent Inflammatory Pain-Induced Alcohol Relapse-Like Rat …

2021

Evidence concerning the role of alcohol-induced neuroinflammation in alcohol intake and relapse has increased in the last few years. It is also proven that mu-opioid receptors (MORs) mediate the reinforcing properties of alcohol and, interestingly, previous research suggests that neuroinflammation and MORs could be related. Our objective is to study neuroinflammatory states and microglial activation, together with adaptations on MOR expression in the mesocorticolimbic system (MCLS) during the abstinence and relapse phases. To do so, we have used a sex-dependent rat model of complete Freund’s adjuvant (CFA)-induced alcohol deprivation effect (ADE). Firstly, our results confirm that only CFA-…

Malemedicine.medical_treatmentFreund's AdjuvantReceptors Opioid mualcohol deprivation effectNitric Oxide Synthase Type IImicroglianeuroinflammationRats Sprague-DawleyRecurrenceLimbic SystemImmunology and AllergypainPhosphorylationReceptormedia_commonMicrogliaAlcohol AbstinencealcoholMicrofilament ProteinsNF-kappa BBrief Research ReportInterleukin 10AlcoholismCytokinemedicine.anatomical_structureCytokinesFemaleμ-opioid receptorInflammation Mediatorsmedicine.medical_specialtyNeuroimmunomodulationmedia_common.quotation_subjectImmunologyPrefrontal CortexSex FactorsDownregulation and upregulationInternal medicinemedicineAnimalsNeuroinflammationbusiness.industryCalcium-Binding ProteinsAbstinenceRC581-607EndocrinologyCyclooxygenase 2mu-opioid receptorImmunologic diseases. AllergybusinessFrontiers in Immunology
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