Search results for "DEXAMETHASONE"

showing 10 items of 246 documents

17 beta-carboxamide steroids: highly effective inhibitors of the phytohaemagglutinin mediated blastogenesis of normal human peripheral lymphocytes.

1984

Several novel 17 beta-carboxamide analogues of dexamethasone were synthesized. The common precursor, 9-fluoro-16 alpha-methyl-11 beta,17-dihydroxy-3-oxo-1,4-androstadiene-17 beta-carboxylic acid, did not bind to the glucocorticoid receptors of rat liver and human spleen tumours. In addition, no inhibition of the mitogen-induced blastogenesis of cultured human peripheral lymphocytes was observed. The 17 beta-carboxamide analogues, however, bound with similar affinities to the glucocorticoid receptors of both tissues. They inhibited the mitogen-induced blastogenesis of peripheral lymphocytes, showing the same potency and same order of binding affinity as the natural glucocorticoids.

Malemedicine.medical_specialtyChemical Phenomenamedicine.drug_classClinical BiochemistryeducationCarboxamideBiologyIn Vitro TechniquesLymphocyte ActivationBinding CompetitiveDexamethasoneGlucocorticoid receptorCytosolReceptors GlucocorticoidInternal medicinemedicinePotencyAnimalsHumansPhytohemagglutininsBeta (finance)GlucocorticoidsDexamethasonePhytohaemagglutininBiochemistry (medical)Biological activityRats Inbred StrainsGeneral MedicineDNAPeripheralRatsChemistryEndocrinologyLiverbiology.proteinmedicine.drugThymidineJournal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie
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Regulation of argininosuccinate synthetase level by corticosteroid and pancreatic hormones during perinatal period.

1995

The urea cycle takes place in the hepatocyte of ureothelic animals. The conversion of ammonia into urea involves five reactions. The first 2 take place in the matrix of the mitochondria, the last 2 occur in the cytosol. Argininosuccinate synthetase (AS) is the third reaction of the urea cycle. It catalyses the condensation of citrulline and aspartate into arginonosuccinate. We have previously reported that rat AS activity was present in the cytosol and the outer membrane of the mitochondria. We have shown that, at the activity level, the colocation of AS was changing during fetal and neonatal development and was under the control of corticosteroid and pancreatic hormones. However, an unreso…

Malemedicine.medical_specialtyCytoplasmHydrocortisoneClinical BiochemistryArgininosuccinate synthaseMitochondria LiverMitochondrionArgininosuccinate SynthaseDexamethasoneDiabetes Mellitus Experimentalchemistry.chemical_compoundAdrenal Cortex HormonesPregnancyInternal medicinemedicineCitrullineAnimalsRats WistarMolecular BiologyPancreatic hormoneCells CulturedHypophysectomybiologyAdrenalectomyCell BiologyGeneral MedicineGlucagonPancreatic HormonesRatsCytosolmedicine.anatomical_structureEndocrinologychemistryAnimals NewbornLiverHepatocyteUrea cyclebiology.proteinFemaleHormoneMolecular and cellular biochemistry
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An experimental comparative study of dexamethasone, melatonin and tacrolimus in noise-induced hearing loss.

2008

The calcineurin inhibitor tacrolimus (TCR) and the pineal gland hormone and antioxidant melatonin (MLT) have been shown to possess otoprotective properties against noise-induced hearing loss (NIHL). In contrast, dexamethasone (DXM) was not effective as an otoprotective agent against NIHL. Further studies are needed to understand the exact molecular mechanisms involved.Exposure to noise pollution and use of audio devices for long periods of time at high volume is known to cause hearing loss or NIHL. Our goal was to evaluate the effectiveness of various known compounds such as the anti-inflammatory DXM, the antioxidant MLT and the immunosuppressant TCR against NIHL.Thirty-two Wistar rats were…

Malemedicine.medical_specialtyHearing lossOtoacoustic Emissions SpontaneousAnti-Inflammatory AgentsAntioxidantsDexamethasoneTacrolimusMelatoninPineal glandInternal medicineotorhinolaryngologic diseasesmedicineEvoked Potentials Auditory Brain StemAnimalsRats WistarDexamethasoneMelatoninbusiness.industryReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaGeneral Medicinemedicine.diseaseTacrolimusRatsCalcineurinHair Cells Auditory OuterEndocrinologymedicine.anatomical_structureOtorhinolaryngologyHearing Loss Noise-Inducedmedicine.symptombusinessProto-Oncogene Proteins c-fosNoise-induced hearing lossImmunosuppressive AgentsHormonemedicine.drugActa oto-laryngologica
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Glucocorticoids as modulators of expression and activity of Antithrombin (At): potential clinical relevance.

2014

Abstract Introduction An inverse relationship has been reported between decreased postoperative Antithrombin (AT) plasmatic levels and the incidence of complications. We hypothesized that Nuclear Hormone Receptors could modulate the expression of SERPINC1 , encoding AT, through a Hormone Regulatory Element present in its promoter, and thus hormone analogs could be a pharmacological complement in surgical procedures to activate endogenous AT synthesis. Materials and Methods The expression of SERPINC1 was analyzed in HepG2 cells by quantitative RT-PCR and Western Blot. Two studies were conducted with (a) patients submitted to cardiac surgery with cardiopulmonary bypass receiving (n =17) or no…

Malemedicine.medical_specialtyMolecular Sequence DataReceptors Cytoplasmic and NuclearRetinoid X receptorLigandsAntithrombinsCohort StudiesRetinoidsInternal medicinemedicineHumansGlucocorticoidsDexamethasoneAgedCardiopulmonary BypassBase Sequencebusiness.industryAntithrombinRNA-Binding ProteinsHematologyHep G2 CellsIsoxazolesMiddle AgedEndocrinologyRetinoid X ReceptorsTreatment OutcomeMethylprednisoloneNuclear receptorHemostasisFemaleCortisonebusinessHormonemedicine.drugThrombosis research
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Effects of glucocorticoid excess on the sensitivity of glucose transport and metabolism to insulin in rat skeletal muscle.

1997

This study examines the mechanisms of glucocorticoid-induced insulin resistance in rat soleus muscle. Glucocorticoid excess was induced by administration of dexamethasone to rats for 5 days. Dexamethasone decreased the sensitivity of 3-O-methylglucose transport, 2-deoxyglucose phosphorylation, glycogen synthesis and glucose oxidation to insulin. The total content of GLUT4 glucose transporters was not decreased by dexamethasone; however, the increase in these transporters in the plasma membrane in response to insulin (100 m-units/litre) was lessened. In contrast, the sensitivity of lactate formation to insulin was normal. The content of 2-deoxyglucose in the dexamethasone-treated muscle was …

Malemedicine.medical_specialtyMonosaccharide Transport Proteinsmedicine.medical_treatmentBlotting WesternGlucose-6-PhosphateMuscle ProteinsDeoxyglucoseBiochemistryDexamethasonechemistry.chemical_compoundInsulin resistanceInternal medicineHexokinasemedicineFructosediphosphatesAnimalsInsulinGlycolysisLactic AcidPhosphorylationRats WistarGlycogen synthaseMuscle SkeletalMolecular BiologyGlucocorticoidsHexokinaseGlucose Transporter Type 4biologyInsulinGlucose transporterCell BiologyMetabolismmedicine.diseaseRatsEndocrinologyGlucosechemistrybiology.protein3-O-MethylglucoseGLUT4GlycogenResearch Article
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Down-regulation of the expression of endothelial NO synthase is likely to contribute to glucocorticoid-mediated hypertension.

1999

Hypertension is a side effect of systemically administered glucocorticoids, but the underlying molecular mechanism remains poorly understood. Ingestion of dexamethasone by rats telemetrically instrumented increased blood pressure progressively over 7 days. Plasma concentrations of Na + and K + and urinary Na + and K + excretion remained constant, excluding a mineralocorticoid-mediated mechanism. Plasma NO 2 − /NO 3 − (the oxidation products of NO) decreased to 40%, and the expression of endothelial NO synthase (NOS III) was found down-regulated in the aorta and several other tissues of glucocorticoid-treated rats. The vasodilator response of resistance arterioles was tested by intravital m…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIDown-RegulationVasodilationBiologyEndothelial NOSRats Inbred WKYUmbilical veinDexamethasonechemistry.chemical_compoundInternal medicinemedicineAnimalsRNA MessengerPromoter Regions GeneticAortaCells CulturedNitritesDNA PrimersMultidisciplinaryNitratesBase SequenceAntiglucocorticoidNitric Oxide Synthase Type IIIBiological SciencesRatsNitric oxide synthaseVasodilationEndocrinologychemistryHypertensionbiology.proteinEndothelium VascularNitric Oxide SynthaseGlucocorticoidIntravital microscopymedicine.drugTranscription FactorsProceedings of the National Academy of Sciences of the United States of America
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Correlation between the effects of retinoic acid and dexamethasone on liver tyrosine aminotransferase

1997

A single dose of 50 microg of trans-retinoic acid administered to rats significantly raised the level of hepatic tyrosine after a few hours. This effect was compared with that of dexamethasone and a possible correlation between these effectors was also investigated. An equal increase in enzyme activity level caused by retinoic acid was observed in adrenalectomized rats, leading to the suggestion that the effect of retinoic acid on liver tyrosine aminotransferase is independent of glucocorticoids. However, the study of the binding activity of the liver nuclear glucocorticoid receptors vs dexamethasone showed that this activity is favoured by retinoic acid, whereas no variation was evidenced …

Malemedicine.medical_specialtyReceptors Retinoic AcidEndocrinology Diabetes and MetabolismClinical BiochemistryTyrosine TransaminaseRetinoic acidretinoic acid receptorAntineoplastic AgentsTretinoindexamethasoneBiologyBiochemistrychemistry.chemical_compoundReceptors GlucocorticoidEndocrinologyGlucocorticoid receptorTyrosine aminotransferaseInternal medicineglucocorticoid receptorretinoic acidmedicineAnimalsRats WistarTyrosineReceptorMolecular BiologyDexamethasoneTyrosine TransaminaseBinding SitesAdrenalectomyCell BiologyRatsEndocrinologyLiverchemistryTyrosineMolecular Medicinetyrosine aminotransferaseInjections IntraperitonealGlucocorticoidmedicine.drug
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Local safety of repeated intravitreal Ozurdex

2013

Sir, The article entitled ‘Twelve-month experience with Ozurdex for the treatment of macular edema associated with retinal vein occlusion'1 highlights the significant cataract progression in eyes receiving more than one Ozurdex implant. We retrospectively reviewed the charts of all patients with macular edema secondary to retinal vein occlusion (RVO) refractory to current therapies and treated with Ozurdex from April 2010 until March 2012. The mean age of patients with branch RVO (n=33) was 72.4. In eyes receiving a second Ozurdex implant, four out of the five phakic eyes showed progression of cataract requiring surgery. We registered one case of anterior chamber migration resulting in a bu…

Malemedicine.medical_specialtyRetinal Veingenetic structuresDexamethasoneMacular EdemaRefractoryOphthalmologyCorrespondenceRetinal Vein OcclusionOcclusionmedicineHumansIn patientGlucocorticoidsMacular edemaDexamethasonebusiness.industryIncidence (epidemiology)medicine.diseaseeye diseasesSurgeryOphthalmologyFemalesense organsImplantbusinessmedicine.drugEye
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Permissive and suppressive effects of dexamethasone on enzyme induction in hepatocyte co-cultures.

2002

1. Steroids are known to act as permissive factors in hepatocytes. This study shows that dexamethasone (DEX) is a permissive factor for induction of CYP2B1/2, CYP3A1, CYP2A1 and probably also CYP2C11 in cultures with primary rat hepatocytes. 2. The induction factor of phenobarbital (PB)-induced formation of 16beta-hydroxytestosterone (OHT), a testosterone biotransformation product predominantly formed by CYP2B1, is increased 18-fold by the addition of 32 nM DEX to the culture medium. Interestingly, higher concentrations of DEX up to 1000 nM led to a concentration-dependent maximally 5-fold decrease (p = 0.002) of phenobarbital-induced 16beta-OHT formation compared with the effect observed w…

Malemedicine.medical_specialtyTime FactorsHealth Toxicology and MutagenesisAnti-Inflammatory AgentsBiologyToxicologyBiochemistryDexamethasoneRats Sprague-DawleyEnzyme activatorInternal medicinepolycyclic compoundsmedicineCytochrome P-450 CYP1A1AnimalsCytochrome P-450 CYP3AProtein IsoformsPermissiveEnzyme inducerCytochrome P450 Family 2DexamethasoneCells CulturedPharmacologyCryopreservationDose-Response Relationship DrugBiological activityGeneral MedicineIn vitroCoculture TechniquesRatsEnzyme ActivationEndocrinologymedicine.anatomical_structureLiverSteroid 16-alpha-HydroxylaseHepatocytePhenobarbitalCytochrome P-450 CYP2B1Steroid Hydroxylasesbiology.proteinHepatocytesHydroxytestosteronesAryl Hydrocarbon HydroxylasesExcitatory Amino Acid Antagonistshormones hormone substitutes and hormone antagonistsGlucocorticoidmedicine.drugXenobiotica; the fate of foreign compounds in biological systems
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Dexamethasone upregulates Nox1 expression in vascular smooth muscle cells.

2014

<b><i>Background/Aim:</i></b> It has been demonstrated that dexamethasone-induced hypertension can be prevented by the NADPH oxidase inhibitor apocynin. The effect of dexamethasone on NADPH oxidase, however, is unknown. The present study was conducted to investigate the effect of dexamethasone on the gene expression of Nox1, the major NADPH oxidase isoform in vascular smooth muscle cells. <b><i>Results:</i></b> Oral treatment of Wistar-Kyoto rats with dexamethasone (0.03 mg/kg/day) for 12 days led to an upregulation of Nox1 mRNA expression in the aorta. In cultured A7r5 rat aortic smooth muscle cells, dexamethasone increased Nox1 mRNA expressi…

Malemedicine.medical_specialtyVascular smooth muscleTime FactorsMyocytes Smooth Musclemedicine.disease_causeRats Inbred WKYDexamethasoneHistone DeacetylasesMuscle Smooth Vascularchemistry.chemical_compoundReceptors GlucocorticoidInternal medicinemedicineAnimalsNADH NADPH Oxidoreductasescardiovascular diseasesRNA MessengerGlucocorticoidsDexamethasoneAortaPharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyDose-Response Relationship DrugChemistryfungifood and beveragesGeneral MedicineRatsUp-RegulationEndocrinologyNOX1Gene Knockdown TechniquesApocynincardiovascular systembiology.proteinNADPH Oxidase 1Oxidative stresscirculatory and respiratory physiologymedicine.drugPharmacology
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