Search results for "Wistar"

showing 10 items of 1094 documents

Pharmacokinetic Interaction between Nevirapine and Nortriptyline in Rats: Inhibition of Nevirapine Metabolism by Nortriptyline

2014

ABSTRACTOne of the most frequent comorbidities of HIV infection is depression, with a lifetime prevalence of 22 to 45%. Therefore, it was decided to study a potential pharmacokinetic interaction between the nonnucleoside reverse transcriptase inhibitor nevirapine (NVP) and the tricyclic antidepressant nortriptyline (NT). NVP and NT were administered to rats either orally, intraduodenally, or intravenously, and the changes in plasma levels and pharmacokinetic parameters were analyzed. Experiments with rat and human hepatic microsomes were carried out to evaluate the inhibitory effects of NT on NVP metabolism. NVP plasma concentrations were significantly higher when this drug was coadminister…

MaleNevirapineAnti-HIV AgentsAdministration OralNortriptylineAntidepressive Agents TricyclicPharmacologyPharmacokineticsimmune system diseasesIn vivomedicineAnimalsHumansPharmacology (medical)NevirapineRats WistarBiotransformationPharmacologyDose-Response Relationship DrugReverse-transcriptase inhibitorbusiness.industryvirus diseasesRatsDose–response relationshipInfectious DiseasesArea Under CurveInjections IntravenousMicrosomes LiverMicrosomeReverse Transcriptase InhibitorsNortriptylinebusinessDrug AntagonismDrug metabolismmedicine.drugAntimicrobial Agents and Chemotherapy
researchProduct

Effects of nicotinamide on central cholinergic transmission and on spatial learning in rats

1996

High-dose nicotinamide (1000 mg/kg) leads to a minor increase of plasma choline but to a major increase of the choline concentrations in the intra- and extracellular spaces of the brain. In the hippocampus, the nicotinamide-induced increase in choline was associated with an increase in the release of acetylcholine under stimulated conditions. In young rats, nicotinamide in doses between 10 and 1000 mg/kg did not influence spatial learning, as tested in the Morris water maze. In old rats, low doses of nicotinamide were ineffective whereas the high dose of 1000 mg/kg even impaired spatial learning. The combined administration of choline and nicotinamide had a synergistic effect on brain choli…

MaleNiacinamideAgingClinical BiochemistryHippocampusMorris water navigation taskMotor ActivityPharmacologyToxicologyHippocampusSynaptic TransmissionBiochemistryCholineBehavioral Neurosciencechemistry.chemical_compoundCognitionParasympathetic Nervous SystemmedicineExtracellularAnimalsCholineRats WistarMaze LearningBiological PsychiatryBrain ChemistryPharmacologyNicotinamideBiological activityAcetylcholineRatschemistryBiochemistryCholinergicExtracellular SpaceAcetylcholinemedicine.drugPharmacology Biochemistry and Behavior
researchProduct

Inhibitors of poly (ADP-ribose) synthetase reduce renal ischemia-reperfusion injury in the anesthetized rat in vivo.

2000

The activation of poly (ADP-ribose) synthetase (PARS) subsequent to DNA damage caused by reactive oxygen or nitrogen species has been implicated in several pathophysiological conditions, including ischemia-reperfusion injury and shock. The aim of this study was to investigate whether PARS inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo. Male Wistar rats were subjected to 45 min bilateral clamping of the renal pedicles, followed by 6 h reperfusion (control animals). Animals were administered the PARS inhibitors 3-aminobenzamide, 1, 5-dihydroxyisoquinoline, or nicotinamide during the reperfusion period. Ischemia, followed by reperfusion, produc…

MaleNiacinamideIschemiaRenal functionNatriuresisKidney; Poly (ADP-ribose) synthetase inhibitors; Proximal tubule; Reactive oxygen species; Reperfusion injuryPharmacologyPoly(ADP-ribose) Polymerase InhibitorsKidneyBiochemistryExcretionchemistry.chemical_compoundIn vivoGeneticsmedicineAnimalsUreaAnesthesiaEnzyme InhibitorsRats WistarMolecular BiologyKidneyCreatinineNicotinamidemedicine.diseaseIsoquinolinesRatsOxidative Stressmedicine.anatomical_structurechemistryCreatinineReperfusion InjuryBenzamidesReactive Oxygen SpeciesReperfusion injuryBiotechnologyGlomerular Filtration RateFASEB journal : official publication of the Federation of American Societies for Experimental Biology
researchProduct

Regulation of free choline in rat brain: dietary and pharmacological manipulations.

1998

The present study analyses, comparatively, the kinetics of free choline in the brain of rats during dietary and pharmacological manipulations. Low-choline diet halved the choline plasma level but did not cause significant changes of CSF choline. High-choline diet, hypoxia and treatment with nicotinamide increased brain choline availability through a central site of action and increased the CSF choline concentration. CSF choline concentrations were more effectively elevated by nicotinamide treatment (20-25 microM) than by acute choline administration (13-15 microM). Increases of CSF choline, due to brain choline mobilization, were consistently associated with a net release of choline from th…

MaleNiacinamidemedicine.medical_specialtyCerebral arteriesCentral nervous systemBiological AvailabilityBiologyCholineCellular and Molecular Neurosciencechemistry.chemical_compoundInternal medicinemedicineCholineAnimalsRats WistarHypoxiaNicotinamideOsmolar ConcentrationBrainCell BiologyVenous bloodHypoxia (medical)Cerebral ArteriesCerebral VeinsDietRatsEndocrinologymedicine.anatomical_structurechemistrymedicine.symptomAcetylcholineHomeostasismedicine.drugNeurochemistry international
researchProduct

Enhancement of brain choline levels by nicotinamide: mechanism of action

1998

Following the subcutaneous (s.c.) administration of nicotinamide (10 mmol/kg), the brain and CSF levels of nicotinamide were increased to millimolar concentrations, but the concentrations of N-methylnicotinamide (NMN) in the CSF, and of NMN and NAD+ in brain tissue were not significantly altered. Concomitantly, nicotinamide caused increases of the choline levels in the venous brain blood. In hippocampal slices, nicotinamide (1-10 mM) induced choline release in a calcium- and mepacrine-sensitive manner and, in [3H]choline-labelled slices, increased the levels of [3H]lyso-phosphatidylcholine and [3H]glycerophosphocholine. We conclude that nicotinamide enhances brain choline concentrations by …

MaleNiacinamidemedicine.medical_specialtyTime FactorsInjections Subcutaneouschemistry.chemical_elementIn Vitro TechniquesCalciumHippocampusCholinechemistry.chemical_compoundPhospholipase A2Internal medicinemedicineAnimalsCholineRats WistarPhospholipase AbiologyNicotinamideGeneral NeuroscienceBrainNADRatsB vitaminsEndocrinologyLiverchemistryNiacinamidebiology.proteinNAD+ kinaseNeuroscience Letters
researchProduct

Transcription factor gene expression profiling after acute intermittent nicotine treatment in the rat cerebral cortex

2004

Several studies in different in vitro and in vivo models have demonstrated neuroprotective effects of nicotinic receptor agonists and indirect trophic actions of nicotine on brain are suggested from observations describing nicotine as a cognitive enhancer by increasing vigilance and improving learning and memory. While an increasing number of studies have given evidence of neuroprotective and neurotrophic effects of nicotine treatment, the molecular mechanism mediating the neurotrophic effects of nicotine are not fully understood. Previously in an analysis of several neurotrophic factors as possible mediators of nicotine-induced neuroprotection and/or neurotrophic effects we could reveal th…

MaleNicotineGene ExpressionBiologyNeuroprotectionNicotineCerebral Cortex/drug effectNeurotrophic factorsmedicineAnimalsNicotinic AgonistsRats WistarIn Situ HybridizationOligonucleotide Array Sequence AnalysisCerebral CortexMicroarray analysis techniquesGene Expression ProfilingGeneral NeuroscienceRatsGene expression profilingNicotinic agonistNicotine/pharmacology Nicotinic Agonistsbiology.proteinGene Expression/drug effectImmediate early geneNeuroscienceTranscription Factorsmedicine.drugNeurotrophinNeuroscience
researchProduct

Acute intermittent nicotine treatment induces fibroblast growth factor-2 in the subventricular zone of the adult rat brain and enhances neuronal prec…

2007

Abstract Over the past years, evidence has accumulated that stem cells are present in the adult brain, and generate neurons and/or glia from two active germinal zones: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus. This study shows that acute intermittent nicotine treatment significantly enhances neuronal precursor cell proliferation in the SVZ of adult rat brain, but not in the SGZ of the hippocampus, and pre-treatment with mecamylamine, a nonselective nAChR antagonist, blocks the enhanced precursor proliferation by nicotine. This effect is supported by up-regulation of fibroblast growth factor-2 (FGF-2) mRNA …

MaleNicotinemedicine.medical_specialtyBasic fibroblast growth factorSubventricular zoneNicotinic AntagonistsReceptors NicotinicBiologyFibroblast growth factorSettore BIO/09 - FisiologiaHippocampusSubgranular zonechemistry.chemical_compoundLateral VentriclesInternal medicinePrecursor cellmedicineAnimalsPyrrolesNicotinic AgonistsRNA MessengerReceptor Fibroblast Growth Factor Type 1Rats WistarCell ProliferationNeuronsNeuronal PlasticityStem CellsGeneral NeuroscienceFibroblast growth factor receptor 1Dentate gyrusNeurogenesisCell DifferentiationNerve RegenerationRatsUp-RegulationCell biologymedicine.anatomical_structureEndocrinologynervous systemchemistryneurogenesis FGF-2 FGFR-1 subventricular zone nicotineFibroblast Growth Factor 2Neuroscience
researchProduct

Neuroprotective Properties of Mildronate, a Small Molecule, in a Rat Model of Parkinson’s Disease

2010

Previously, we have found that mildronate [3-(2,2,2-trimethylhydrazinium) propionate dihydrate], a small molecule with charged nitrogen and oxygen atoms, protects mitochondrial metabolism that is altered by inhibitors of complex I and has neuroprotective effects in an azidothymidine-neurotoxicity mouse model. In the present study, we investigated the effects of mildronate in a rat model of Parkinson’s disease (PD) that was generated via a unilateral intrastriatal injection of the neurotoxin 6-hydroxydopamine (6‑OHDA). We assessed the expression of cell biomarkers that are involved in signaling cascades and provide neural and glial integration: the neuronal marker TH (tyrosine hydroxylase); …

MaleNitric Oxide Synthase Type IIlcsh:ChemistryUbiquitinNeurotoxinlcsh:QH301-705.5Receptor Notch3SpectroscopyNeuronsReceptors NotchbiologyGlial fibrillary acidic proteinMicrofilament ProteinsGeneral MedicineComputer Science ApplicationsCell biologySubstantia NigraNitric oxide synthaseNeuroprotective Agentsmedicine.anatomical_structureBiochemistryNeurogliaNeurogliaMethylhydrazinesneuroimmunological biomarkersTyrosine 3-Monooxygenasesmall moleculeSubstantia nigraParkinson’s disease; 6-OHDA model; neuroimmunological biomarkers; mildronate; small moleculeNeuroprotectionArticleCatalysisInorganic ChemistryGlial Fibrillary Acidic ProteinmedicineAnimalsParkinson Disease SecondaryRats WistarPhysical and Theoretical ChemistryOxidopamineMolecular BiologyTyrosine hydroxylase6-OHDA modelCalcium-Binding ProteinsmildronateOrganic ChemistryCorpus StriatumRatslcsh:Biology (General)lcsh:QD1-999nervous systemParkinson’s diseasebiology.proteinBiomarkersInternational Journal of Molecular Sciences
researchProduct

Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-glutathionylation of endothelial nitric oxide synth…

2011

Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT(1))-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S-glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP-cyclohydrolase I.Wistar rats were treated with telmisartan (2.7 or 8 mg/kg per day PO for 10 days) and with GTN (50 mg/kg per day SC for 3 days). Aortic eNOS phos…

MaleNitric Oxide Synthase Type IIIPhysiologyVasodilator AgentsPharmacologyBenzoatesCell LineNitroglycerinmedicineAnimalsHumansTelmisartanEnzyme InhibitorsPhosphorylationRats WistarS-GlutathionylationEndothelial dysfunctionGTP CyclohydrolaseBeneficial effectsNitroglycerinPharmacologyAngiotensin II receptor type 1Dose-Response Relationship DrugEndothelial nitric oxide synthaseChemistryEndothelial CellsDrug ToleranceAldehyde Dehydrogenasemedicine.diseaseGlutathioneMitochondriaRatsVasodilationOxidative StressTetrahydrofolate DehydrogenaseMolecular MedicinePhosphorylationBenzimidazolesEndothelium VascularTelmisartanReactive Oxygen SpeciesAngiotensin II Type 1 Receptor BlockersProtein Processing Post-Translationalmedicine.drugVascular Pharmacology
researchProduct

Reduction of infarct size by the NO donors sodium nitroprusside and spermine/NO after transient focal cerebral ischemia in rats

2000

Nitric oxide (NO) plays a dual role (neuroprotection and neurotoxicity) in cerebral ischemia. NO promoting strategies may be beneficial shortly after ischemia. Therefore, we have studied the hemodynamic and possible neuroprotective effects of two NO donors, the classical nitrovasodilator sodium nitroprusside (SNP) and the NONOate spermine/NO, after transient focal cerebral ischemia in rats. Parietal cortical perfusion was measured by laser-Doppler flowmetry. The effects of increasing intravenous doses (10-300 microgram) of sodium nitroprusside and spermine/NO on cortical perfusion and arterial blood pressure were assessed. Transient (2 h) focal cerebral ischemia was carried out by the intra…

MaleNitroprussideVasodilator AgentsIschemiaSpermineBlood PressurePerfusion scanningBrain damagePharmacologyNitric oxidechemistry.chemical_compoundAnimalsMedicineNitric Oxide DonorsRats WistarMolecular Biologybusiness.industryCerebral infarctionGeneral NeuroscienceBrainCerebral Infarctionmedicine.diseaseRatschemistryIschemic Attack TransientAnesthesiaSpermineNeurology (clinical)Sodium nitroprussidemedicine.symptombusinessNitrovasodilatorDevelopmental Biologymedicine.drugBrain Research
researchProduct