Search results for "HEME OXYGENASE"

showing 10 items of 90 documents

Antioxidant and Antiinflammatory Properties of Heme Oxygenase-1 in Osteoarthritic Articular Cells

2012

Heme oxygenase-1 (HO-1) is induced in cells by various stimuli as a defense system against oxidative stress. It is known that reactive oxygen species (ROS) participates in the initiation and progression of osteoarthritis (OA) and several antioxidant systems may protect cartilage components. HO-1 induction or CO release from CORM-2 counteracts oxidative stress and protects against proinflammatory and catabolic effects of interleukin-1β in OA chondrocytes, osteoblasts, and synoviocytes as well as in OA osteochondral explants. Both approaches have been able to downregulate the production of mediators such as reactive oxygen species, nitric oxide, matrix metalloproteinases, prostaglandin E2, cy…

chemistry.chemical_classificationReactive oxygen speciesCartilagemedicine.disease_causeProinflammatory cytokineCell biologyHeme oxygenasechemistry.chemical_compoundmedicine.anatomical_structurechemistrymedicineProstaglandin E2HemeOxidative stressAggrecanmedicine.drug
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ROLE OF HEME OXYGENASE-1 (HSP32) AND HSP90 IN GLIOBLASTOMA

2017

Glioblastoma (GBM) is the most common and malignant primary brain tumor in adults. The current treatment regimes for glioblastoma demonstrated a low efficiency and offer a poor prognosis. Advancements in conventional treatment strategies have only yielded modest improvements in overall survival. The heat shockproteins, heme oxygenase-1 (HO-1) and Hsp90, serve these pivotal roles in tumor cells and have been identified as effective targets for developing therapeutics. This topic review summarizes the current preclinical and clinical evidences and rationale to define the potential of HO-1 and Hsp90 in GBM progression and chemoresistance.

lcsh:R5-920heat shock proteinsmolecular chaperonesglioblastomacancerHsp90heme oxygenaselcsh:Medicine (General)Euromediterranean Biomedical Journal
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A minireview on NHE1 inhibitors. A rediscovered hope in oncohematology.

2015

Background: Na+/H+ exchanger-1 (NHE-1) is involved in pH regulation and is up-regulated in different malignancies. Activation of NHE-1 is one way for allowing cells to avoid intracellular acidification and protect them against apoptosis. Inhibitors of NHE-1 are able to decrease intracellular pH and induce apoptosis. Some statins can also act by partial inhibition of NHE-1. This review presents progress in understanding the mechanisms of action of these inhibitors, connections with certain genetic mutations and acquired treatment resistance, as well as new patents on them. Methods: A MEDLINE search for original and review articles using key terms, Na+/H+ exchanger, leukemia, cariporide, and …

lovastatinlcsh:MedicineApoptosisPharmacologyGuanidinesAmiloridep-glycoproteinhemic and lymphatic diseasesDrug InteractionsSulfonesCation Transport ProteinsSodium-Hydrogen Exchanger 1leukemiaMyeloid leukemiaHydrogen-Ion ConcentrationSorafenibUp-RegulationLeukemiaLeukemia Myeloid AcuteImatinib MesylateSignal transductionTyrosine kinasemedicine.drugSignal TransductionSorafenibNiacinamideisoprenylationSodium-Hydrogen Exchangersbcr/ablAntineoplastic AgentsGenes ablGeneral Biochemistry Genetics and Molecular BiologystatinsPatents as TopicCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansProtein Kinase Inhibitorscariporidena+/h+ exchangerTumor hypoxiabusiness.industryPhenylurea Compoundslcsh:ROsmolar Concentrationintracellular phmedicine.diseaseImatinib mesylatefms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3MutationCancer researchTumor Hypoxiaflt3/itdHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessHeme Oxygenase-1DNA DamageBiomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
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Pentaerithrityl tetranitrate improves angiotensin II induced vascular dysfunction via induction of heme oxygenase-1

2010

The organic nitrate pentaerythritol tetranitrate is devoid of nitrate tolerance, which has been attributed to the induction of the antioxidant enzyme heme oxygenase (HO)-1. With the present study, we tested whether chronic treatment with pentaerythritol tetranitrate can improve angiotensin II–induced vascular oxidative stress and dysfunction. In contrast to isosorbide-5 mononitrate (75 mg/kg per day for 7 days), treatment with pentaerythritol tetranitrate (15 mg/kg per day for 7 days) improved the impaired endothelial and smooth muscle function and normalized vascular and cardiac reactive oxygen species production (mitochondria, NADPH oxidase activity, and uncoupled endothelial NO synthase)…

medicine.medical_specialtyAntioxidantNitric Oxide Synthase Type IIImedicine.medical_treatmentVasodilator AgentsBlotting WesternFluorescent Antibody TechniquePentaerythritol tetranitratemedicine.disease_causePentaerythritolArticlechemistry.chemical_compoundInternal medicineRats Inbred SHRInternal MedicinemedicineAnimalsPentaerythritol TetranitrateEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesAnalysis of VarianceAngiotensin IImedicine.diseaseAngiotensin IIMitochondriaRatsHeme oxygenaseOxidative StressEndocrinologychemistryHeminEndothelium VascularReactive Oxygen SpeciesOxidative stressHeme Oxygenase-1
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Oxidative stress in vascular disease and its pharmacological prevention

2013

Cardiovascular risk factors lead to enhanced production of reactive oxygen species (ROS) generated by NADPH oxidase, xanthine oxidase (XO), the mitochondrial electron-transport chain (ETC), and dysfunctional endothelial nitric oxide synthase (eNOS). When the capacity of antioxidant defense systems [e.g., superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), heme oxygenase (HO), paraoxonase (PON)] is exceeded, this results in oxidative stress, which can promote atherogenesis. Therefore, pharmacological means to prevent oxidative stress are of major therapeutic interest. Some established drugs and novel therapeutic approaches can prevent oxidative stress and, presumably, vascula…

medicine.medical_specialtyAntioxidantmedicine.medical_treatmentToxicologymedicine.disease_causeAntioxidantsSuperoxide dismutasechemistry.chemical_compoundInternal medicinemedicineAnimalsHumansVascular DiseasesXanthine oxidasePharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyGlutathione peroxidaseHeme oxygenaseOxidative StressEndocrinologychemistrybiology.proteinOxidative stressTrends in Pharmacological Sciences
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Disturbed Lipid Metabolism in Diabetic Patients with Manifest Coronary Artery Disease Is Associated with Enhanced Inflammation

2021

Background: Diabetic vasculopathy plays an important role in the pathophysiology of coronary artery disease (CAD) with oxidative stress as a strong mediator. This study aims to elucidate the underlying pathomechanisms of diabetic cardiac vasculopathy leading to coronary disease with an emphasis on the role of oxidative stress. Therefore, novel insights into antioxidant pathways might contribute to new strategies in the treatment and prevention of diabetic CAD. Methods: In 20 patients with insulin-dependent or non-insulin dependent diabetes mellitus (IDDM/NIDDM) and 39 non-diabetic (CTR) patients, myocardial markers of oxidative stress, vasoactive proteins, endothelial nitric oxide synthase …

medicine.medical_specialtyHealth Toxicology and MutagenesisInflammationmedicine.disease_causeArticleCoronary artery diseaseEnosDiabetes mellitusInternal medicinemedicineHumansoxidative stressbiologybusiness.industrydyslipidemiaPublic Health Environmental and Occupational HealthRLipid metabolismLipid Metabolismmedicine.diseasebiology.organism_classificationHeme oxygenaseEndocrinologynutritionDiabetes Mellitus Type 2inflammationdiabetes mellitusMedicinemedicine.symptombusinesschronic diseaseDiabetic AngiopathiesOxidative stressDyslipidemiacoronary artery diseaseInternational Journal of Environmental Research and Public Health
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Abstract 18540: Heme Oxygenase 1 Activity and Expression Suppresses a Proinflammatory Phenotype in Monocytes and Correlates With Endothelial Function…

2014

Background: Heme oxygenase-1 (HO-1) confers protection to the vasculature and suppresses inflammatory properties of monocytes and macrophages. It is unclear how HO-1 activity and expression determine the extent of vascular dysfunction in mice and humans. Methods and results: Decreasing HO activity was parallelled by decreasing aortic HO-1, eNOS and phospho-eNOS (ser1177) protein expression in HO-1 deficient mice, whereas aortic expression of nox2 showed a stepwise increase in HO-1+/- and HO-1-/- mice as compared to HO-1+/+ controls. Aortic superoxide formation increased depending on the extent of HO-1 deficiency and was blunted by the PKC inhibitor chelerythrine, indicating activation of t…

medicine.medical_specialtyNADPH oxidasebiologybusiness.industryMonocyteCD14biology.organism_classificationAngiotensin IIProinflammatory cytokineHeme oxygenaseEndocrinologymedicine.anatomical_structureIntegrin alpha MEnosPhysiology (medical)Internal medicineImmunologybiology.proteinmedicineCardiology and Cardiovascular MedicinebusinessCirculation
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Comparative cytoprotective effects of carbocysteine and fluticasone propionate in cigarette smoke extract-stimulated bronchial epithelial cells

2013

Cigarette smoke extracts (CSE) induce oxidative stress, an important feature in chronic obstructive pulmonary disease (COPD), and oxidative stress contributes to the poor clinical efficacy of corticosteroids in COPD patients. Carbocysteine, an antioxidant and mucolytic agent, is effec- tive in reducing the severity and the rate of exacerbations in COPD patients. The effects of carbocysteine on CSE-induced oxidative stress in bronchial epithelial cells as well as the comparison of these antioxidant effects of carbocysteine with those of fluticasone propionate are unknown. The present study was aimed to assess the effects of carbocysteine (10−4 M) in cell survival and intracellular reactive o…

medicine.medical_specialtyNecrosisCell SurvivalNF-E2-Related Factor 2Histone Deacetylase 2ApoptosisSettore MED/10 - Malattie Dell'Apparato Respiratoriomedicine.disease_causeBiochemistryFluticasone propionateAntioxidantsCell Linechemistry.chemical_compoundNecrosisInternal medicineparasitic diseasesTobaccomedicineHumansFluticasonechemistry.chemical_classificationReactive oxygen speciesOriginal PaperPlant ExtractsCarbocysteineCarbocysteineEpithelial CellsCell BiologyGlutathioneCigarette smoke . Airway epithelial cells . Reactive oxygen speciesGlutathioneAndrostadienesOxidative StressEndocrinologychemistryApoptosisFluticasonemedicine.symptomReactive Oxygen SpeciesOxidative stressHeme Oxygenase-1medicine.drug
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

2008

Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…

musculoskeletal diseasesmedicine.medical_treatmentImmunologyAnti-Inflammatory AgentsDrug Evaluation PreclinicalType II collagenArthritisInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]DinoprostoneGeneral Biochemistry Genetics and Molecular BiologyMiceRheumatologyOrganometallic CompoundsPerception and Action [DCN 1]medicineAnimalsImmunology and AllergyChronic inflammation and autoimmunity [UMCN 4.2]Dose-Response Relationship Drugbiologybusiness.industryRANK LigandInterleukinIntercellular Adhesion Molecule-1medicine.diseaseArthritis ExperimentalPathogenesis and modulation of inflammation [N4i 1]Cellular infiltrationCyclooxygenase 2Mice Inbred DBARANKLImmunologybiology.proteinCytokinesTumor necrosis factor alphaMicrobial pathogenesis and host defense [UMCN 4.1]Inflammation Mediatorsmedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1Immunity infection and tissue repair [NCMLS 1]Prostaglandin E
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