Search results for "HEME OXYGENASE-1"

showing 10 items of 57 documents

Atorvastatin treatment increases plasma bilirubin but not HMOX1 expression in stable angina patients.

2015

In vitro and animal studies indicate that statins increase heme oxygenase-1 gene (HMOX1) expression, which then, presumably, increases plasma bilirubin concentration. However, clinical confirmation that statins concomitantly increase HMOX1 expression and plasma bilirubin concentration is lacking. We hypothesized that in patients with stable angina atorvastatin therapy (20 mg/day for 10 weeks) concomitantly increases total bilirubin concentration and HMOX1 expression, as assessed non-invasively by plasma analysis.In 44 patients with stable angina plasma concentrations of total bilirubin, HMOX1 mRNA and HMOX1 protein were measured before and after the statin treatment, as well as plasma conce…

Malemedicine.medical_specialtyHMOX1BilirubinAtorvastatinClinical BiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundInternal medicinemedicineAtorvastatinHumanscardiovascular diseasesAngina StableRNA MessengerIncreased total bilirubinHemeBilirubinGeneral MedicineMiddle AgedMalondialdehydeEndocrinologychemistryProteolysislipids (amino acids peptides and proteins)FemaleAnimal studiesHeme Oxygenase-1Lipoproteinmedicine.drugScandinavian journal of clinical and laboratory investigation
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Heme oxygenase-1 mediates protective effects on inflammatory, catabolic and senescence responses induced by interleukin-1β in osteoarthritic osteobla…

2011

Osteoarthritis (OA) is a chronic degenerative joint disease showing altered bone metabolism. Osteoblasts contribute to the regulation of cartilage metabolism and bone remodeling. We have shown previously that induction of heme oxygenase-1 (HO-1) protects OA cartilage against inflammatory and degradative responses. In this study, we investigated the effects of HO-1 induction on OA osteoblast metabolism. HO-1 was induced with cobalt protoporphyrin IX (CoPP) and by transduction with LV-HO-1. In osteoblasts stimulated with interleukin (IL)-1β, CoPP enhanced mineralization, the expression of a number of markers of osteoblast differentiation such as Runx2, bone morphogenetic protein-2, osteocalci…

Malemedicine.medical_specialtyInterleukin-1betaCartilage metabolismBiochemistryBone remodelingOsteoprotegerinInternal medicineOsteoarthritismedicineHumansCells CulturedCellular SenescenceOsteitisAgedPharmacologyOsteoblastsbiologyChemistryInterleukinOsteoblastMiddle AgedCOPPHeme oxygenaseMetabolismmedicine.anatomical_structureEndocrinologyOsteocalcinbiology.proteinFemaleInflammation MediatorsHeme Oxygenase-1Biochemical Pharmacology
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Hsp60 and heme oxygenase-1 (Hsp32) in acute myocardial infarction

2011

Heat shock proteins (Hsps) are produced in response to various stressors, including ischemia-reperfusion, and they can exit cells and reach the blood. In this pilot study, we determined serum levels of Hsp60 and heme-oxygenase-1 (HO-1; also named Hsp32) in subjects with acute myocardial infarction (AMI) to assess their clinical significance and potential prognostic value. We also performed a bioinformatics analysis of the 2 molecules in search of structural clues on the mechanism of their release from cells. We studied 40 patients consecutively admitted for AMI (male:female patient ratio = 20:20, mean age: 64 ± 13 years) and 40 matched controls. A blood sample was drawn for biochemical anal…

Malemedicine.medical_specialtyPathologyStatistics as TopicMyocardial InfarctionPilot ProjectsCreatineGastroenterologyCoronary artery diseasePathogenesischemistry.chemical_compoundPredictive Value of TestsPhysiology (medical)Internal medicinemedicineHumansClinical significancecardiovascular diseasesMyocardial infarctionacute myocardial infarction heme oxyenase-1 Hsp Hsp60AgedAged 80 and overbiologybusiness.industrySettore BIO/16 - Anatomia UmanaBiochemistry (medical)C-reactive proteinPublic Health Environmental and Occupational HealthCase-control studyComputational BiologyChaperonin 60General MedicineMiddle Agedmedicine.diseaseTroponinchemistryCase-Control Studiesbiology.proteinFemalebusinessHeme Oxygenase-1Follow-Up Studies
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Protection against 2,4,6-trinitrobenzenesulphonic acid-induced colonic inflammation in mice by the marine products bolinaquinone and petrosaspongioli…

2005

Proinflammatory mediators, namely eicosanoids, reactive oxygen and nitrogen species and cytokines, are clearly involved in the pathogenesis of intestinal bowel disease. bolinaquinone (BQ) and petrosaspongiolide M (PT), two marine products with potent anti-inflammatory action, have been shown to control the production of mediators in acute and chronic inflammatory processes. Hence, we have tested here the hypothesis that BQ and PT could ameliorate inflammation and oxidative stress parameters in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colitis in Balb/c mice. BQ and PT were given orally in doses of 10 or 20mg/kg/day. Treatment of the animals with BQ or PT at the highest dose signifi…

Malemedicine.medical_treatmentAnti-Inflammatory AgentsNitric Oxide Synthase Type IIInflammationNerve Tissue ProteinsPharmacologymedicine.disease_causeBiochemistryProinflammatory cytokinechemistry.chemical_compoundMiceSynaptotagminsDysideamedicineAnimalsOleanolic AcidPharmacologyMice Inbred BALB CMembrane GlycoproteinsbiologySuperoxideNitrotyrosineCalcium-Binding ProteinsInterleukinMembrane ProteinsColitisInflammatory Bowel DiseasesImmunohistochemistryNitric oxide synthasechemistryBiochemistryTrinitrobenzenesulfonic AcidCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesSynaptotagmin IHeme Oxygenase (Decyclizing)biology.proteinmedicine.symptomNitric Oxide SynthaseSesquiterpenesOxidative stressHeme Oxygenase-1Prostaglandin EInterleukin-1Biochemical pharmacology
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Influence of heme oxygenase 1 modulation on the progression of murine collagen-induced arthritis.

2005

Contains fulltext : 48023.pdf (Publisher’s version ) (Closed access) OBJECTIVE: Heme oxygenase 1 (HO-1) can be induced by inflammatory mediators as an adaptive response. The objective of the present study was to determine the consequences of HO-1 modulation in the murine collagen-induced arthritis (CIA) model. METHODS: DBA/1J mice were treated with an inhibitor of HO-1, tin protoporphyrin IX (SnPP), or with an inducer of HO-1, cobalt protoporphyrin IX (CoPP), from day 22 to day 29 after CIA induction. The clinical evolution of disease was monitored visually. At the end of the experiment, joints were examined for histopathologic changes. Cytokine levels in paws were measured by enzyme-linked…

Metalloporphyrinsmedicine.medical_treatmentImmunologyArthritisProtoporphyrinsInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]MiceRheumatologyFibrosismedicinePerception and Action [DCN 1]Immunology and AllergyAnimalsPharmacology (medical)Enzyme InhibitorsChronic inflammation and autoimmunity [UMCN 4.2]biologybusiness.industryMembrane Proteinsmedicine.diseaseCOPPArthritis ExperimentalHeme oxygenaseEnzyme ActivationPathogenesis and modulation of inflammation [N4i 1]Disease Models AnimalCytokineCyclooxygenase 2Mice Inbred DBAProstaglandin-Endoperoxide SynthasesImmunologyChronic DiseaseHeme Oxygenase (Decyclizing)biology.proteinDisease ProgressionTumor necrosis factor alphaJointsCyclooxygenasemedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1
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Mitochondrial oxidative stress and nitrate tolerance – comparison of nitroglycerin and pentaerithrityl tetranitrate in Mn-SOD+/- mice

2006

Abstract Background Chronic therapy with nitroglycerin (GTN) results in a rapid development of nitrate tolerance which is associated with an increased production of reactive oxygen species (ROS). According to recent studies, mitochondrial ROS formation and oxidative inactivation of the organic nitrate bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) play an important role for the development of nitrate and cross-tolerance. Methods Tolerance was induced by infusion of wild type (WT) and heterozygous manganese superoxide dismutase mice (Mn-SOD+/-) with ethanolic solution of GTN (12.5 μg/min/kg for 4 d). For comparison, the tolerance-free pentaerithrityl tetranitrate (PETN, 1…

Mitochondrial ROSMaleHeterozygotelcsh:Diseases of the circulatory (Cardiovascular) systemVasodilator AgentsAldehyde dehydrogenaseOxidative phosphorylationMitochondrionPharmacologyIn Vitro Techniquesmedicine.disease_causeDrug Administration ScheduleMitochondria HeartCell LineSuperoxide dismutaseMiceNitroglycerinmedicineAnimalsHumansPentaerythritol TetranitrateRNA MessengerRats WistarHeart metabolismAortachemistry.chemical_classificationReactive oxygen speciesbiologybusiness.industrySuperoxide DismutaseAldehyde Dehydrogenase MitochondrialBilirubinDrug ToleranceFree Radical ScavengersAldehyde DehydrogenaseAcetylcholineRatsVasodilationOxidative Stresschemistrylcsh:RC666-701Anesthesiabiology.proteinCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressHeme Oxygenase-1Research ArticleBMC Cardiovascular Disorders
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Modulation of Nrf2/ARE pathway by food polyphenols: a nutritional neuroprotective strategy for cognitive and neurodegenerative disorders

2011

In recent years, there has been a growing interest, supported by a large number of experimental and epidemi-ological studies, for the beneficial effects of some phenolic substances, contained in commonly used spices and herbs, in preventing various age-related pathologic conditions, ranging from cancer to neurodegenerative diseases. Although the exact mechanisms by which polyphenols promote these effects remain to be elucidated, several reports have shown their ability to stimulate a general xenobiotic response in the target cells, activating multiple defense genes. Data from our and other laboratories have previously demonstrated that curcumin, the yellow pigment of curry, strongly induces…

Programmed cell deathAntioxidantCurcuminNF-E2-Related Factor 2medicine.medical_treatmentCentral nervous systemNeuroscience (miscellaneous)InflammationPharmacologyBiologyResponse ElementsHeterodimers of NF-E2-related factors 2(Nrf2) Antioxidant responsive element (ARE) Heme oxygenase 1 (HO-1) Neurodegenerative disorders Alzheimer’s disease Polyphenols Curcumin (-)- epigallocatechin-3- gallate (EGCG) Brain ageingNeuroprotectionAntioxidantsCatechinArticleCellular and Molecular Neurosciencechemistry.chemical_compoundmedicineAnimalsHumansCognitive declineCaffeic acid phenethyl esterSettore MED/04 - Patologia GeneraleMolecular StructurePolyphenolsNeurodegenerative DiseasesDietmedicine.anatomical_structureNeuroprotective AgentsNeurologyBiochemistrychemistryFoodCurcuminmedicine.symptomCognition DisordersHeme Oxygenase-1
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Altered antioxidant-oxidant status in the aqueous humor and peripheral blood of patients with retinitis pigmentosa.

2013

Retinitis Pigmentosa is a common form of hereditary retinal degeneration constituting the largest Mendelian genetic cause of blindness in the developed world. It has been widely suggested that oxidative stress possibly contributes to its pathogenesis. We measured the levels of total antioxidant capacity, free nitrotyrosine, thiobarbituric acid reactive substances (TBARS) formation, extracellular superoxide dismutase (SOD3) activity, protein, metabolites of the nitric oxide/cyclic GMP pathway, heme oxygenase-I and inducible nitric oxide synthase expression in aqueous humor or/and peripheral blood from fifty-six patients with retinitis pigmentosa and sixty subjects without systemic or ocular …

Retinal degenerationAdultMalePathologymedicine.medical_specialtygenetic structuresSOD3lcsh:MedicineGene ExpressionPharmacologymedicine.disease_causeNitric OxideAntioxidantsNitric oxideAqueous Humorchemistry.chemical_compoundRetinitis pigmentosaTBARSmedicineCluster AnalysisHumanslcsh:ScienceCyclic GMPMultidisciplinarybiologySuperoxide DismutaseNitrotyrosinelcsh:RMiddle Agedmedicine.diseaseOxidantseye diseasesNitric oxide synthasechemistryCase-Control Studiesbiology.proteinLeukocytes MononuclearMetabolomelcsh:QFemalesense organsOxidative stressBiomarkersHeme Oxygenase-1Retinitis PigmentosaResearch ArticlePloS one
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Ex Vivo Tracking of Endogenous CO with a Ruthenium(II) Complex.

2017

[EN] A two-photon fluorescent probe based on a ruthenium(II) vinyl complex is capable of selectively detecting carbon monoxide in cells and ex vivo using mice with a subcutaneous air pouch as a model for inflammation. This probe combines highly selective and sensitive ex vivo detection of endogenous CO in a realistic model with facile, inexpensive synthesis, and displays many advantages over the widely used palladium-based systems.

StereochemistryChemistry MultidisciplinaryFLUORESCENT-PROBEFluorescent-Probechemistry.chemical_elementCarbonylationEndogeny010402 general chemistryFluorogenic probes01 natural sciencesBiochemistryCatalysischemistry.chemical_compoundQUIMICA ORGANICAColloid and Surface ChemistrySelective detectionQUIMICA ANALITICACarbon-MonoxideLIVING CELLSCARBON-MONOXIDEScience & Technology010405 organic chemistryAirSELECTIVE DETECTIONFLUOROGENIC PROBESAIRQUIMICA INORGANICACARBONYLATIONLiving cellsGeneral ChemistryFluorescence0104 chemical sciencesRutheniumChemistrychemistryPhysical SciencesBiophysicsSubcutaneous airHEME OXYGENASE-103 Chemical SciencesCarbonylationHeme Oxygenase-1Ex vivoCarbon monoxidePalladiumJournal of the American Chemical Society
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''Deferoxamine blocks death induced by glutathione depletion in PC 12 cells''

2013

Chouraqui, E. | Leon, A. | Repesse, Y. | Prigent-Tessier, A. | Bouhallab, S. | Bougle, D. | Marie, C. | Duval, D.; International audience; ''The purpose of the present work was to investigate the mechanisms by which glutathione depletion induced by treatment with buthionine sulfoximine (BSO) led within 24-30 h to PC 12 cells apoptosis. Our results showed that treatment by relatively low concentrations (10-30 mu M) of deferoxamine (DFx), a natural iron-specific chelator, almost completely shielded the cells from BSO-induced toxicity and that DFx still remained protective when added up to 9-12 h after BSO treatment. On the other hand, phosphopeptides derived from milk casein and known to carr…

Time FactorsIronApoptosisDeferoxaminePharmacologyIron Chelating AgentsToxicologymedicine.disease_causePC12 Cellschemistry.chemical_compoundOXIDATIVE-STRESSPARKINSONS-DISEASECaseinmedicineAnimalsHomeostasisButhionine sulfoximineButhionine SulfoximineNeuronsCELLULAR IRONDose-Response Relationship DrugbiologyChemistryGeneral NeuroscienceGlutathioneGlutathioneIRON CHELATORRatsDeferoxamineFerritinSYMPATHETIC NEURONSISCHEMIC-STROKEBiochemistryBRAIN IRONCELLULAR IRON''CytoprotectionApoptosisToxicity[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinSERUM DEPRIVATIONHEME OXYGENASE-1NEURODEGENERATIVE DISORDERSOxidative stress''OXIDATIVE-STRESSmedicine.drug
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