Search results for "enzyme inhibitors"

showing 10 items of 559 documents

Opposite motor responses elicited by ethanol in the posterior VTA: The role of acetaldehyde and the non-metabolized fraction of ethanol

2013

Recent electrophysiological evidence suggests that ethanol simultaneously exerts opposite effects on the activity of dopamine (DA) neurons in the ventral tegmental area (VTA) through two parallel mechanisms, one promoting and the other reducing the GABA release onto VTA DA neurons. Here we explore the possible behavioural implications of these findings by investigating the role displayed by acetaldehyde (the main metabolite of ethanol) and the non-metabolized fraction of ethanol in motor activity of rats. We analyse the appearance of motor activation or depression after intra-VTA administration of ethanol in rats subjected to different pharmacological pre-treatments designed to preferential…

MaleMicroinjectionsMetaboliteGABA(A) receptorsAcetaldehydePharmacologyMotor ActivityNon-metabolized fraction of ethanolBicucullineCellular and Molecular Neurosciencechemistry.chemical_compoundDopaminemedicineAnimalsGABA-A Receptor AntagonistsEnzyme InhibitorsRats WistarPharmacologyEthanolDose-Response Relationship DrugEthanolChemistryGABAA receptorVentral Tegmental AreaAcetaldehydeCentral Nervous System DepressantsBicucullineRatsVentral tegmental areaElectrophysiologymedicine.anatomical_structureBiochemistrynervous systemCyanamideVTAmedicine.drug
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Antihypertensive properties of lactoferricin B-derived peptides.

2010

A set of eight lactoferricin B (LfcinB)-derived peptides was examined for inhibitory effects on angiotensin I-converting enzyme (ACE) activity and ACE-dependent vasoconstriction, and their hypotensive effect in spontaneously hypertensive rats (SHR). Peptides were derived from different elongations both at the C-terminal and N-terminal ends of the representative peptide LfcinB(20-25), which is known as the LfcinB antimicrobial core. All of the eight LfcinB-derived peptides showed in vitro inhibitory effects on ACE activity with different IC(50) values. Moreover, seven of them showed ex vivo inhibitory effects on ACE-dependent vasoconstriction. No clear correlation between in vitro and ex viv…

MaleMolecular Sequence DataAngiotensin-Converting Enzyme InhibitorsPeptidyl-Dipeptidase AInhibitory postsynaptic potentialRats Inbred SHRRenin–angiotensin systemmedicineAnimalsHumansAmino Acid SequenceAntihypertensive Agentschemistry.chemical_classificationbiologyLactoferrinChemistryGeneral ChemistryIn vitroBioavailabilityRatsDisease Models AnimalLactoferrinEnzymeMechanism of actionBiochemistryHypertensionbiology.proteinRabbitsmedicine.symptomGeneral Agricultural and Biological SciencesPeptidesVasoconstrictionJournal of agricultural and food chemistry
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Sustained complete hematologic remission after administration of the tyrosine kinase inhibitor imatinib mesylate in a patient with refractory, second…

2002

Abstract Imatinib mesylate, a tyrosine kinase inhibitor targeting bcr-abl, platelet-derived growth factor receptor (PDGF-R), and c-Kit, effectively induces hematologic and cytogenetic remissions in bcr-abl+ chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) with only mild to moderate side effects. Here, we describe the successful treatment of a 64-year-old man with c-Kit+ secondary acute myeloid leukemia (AML) refractory to standard chemotherapy. Upon 2 weeks of imatinib mesylate administration, the patient achieved a complete hematologic remission in peripheral blood. In addition, complete clearance of leukemic blasts in bone marrow and a significant cytogenetic response…

MaleMyeloidmedicine.drug_classmedicine.medical_treatmentImmunologyAntineoplastic AgentsBiochemistryTyrosine-kinase inhibitorPiperazinesBone MarrowRecurrencehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineSecondary Acute Myeloid LeukemiaHumansReceptors Platelet-Derived Growth FactorEnzyme InhibitorsneoplasmsSalvage TherapyChemotherapyAnemia Refractory with Excess of Blastsbusiness.industryAnemia RefractoryDaunorubicinRemission InductionCytarabineMyeloid leukemiaCell BiologyHematologyExonsMiddle Agedmedicine.diseaseNeoplasm ProteinsLeukemiaLeukemia Myeloid AcuteProto-Oncogene Proteins c-kitmedicine.anatomical_structureImatinib mesylatePyrimidinesDrug Resistance NeoplasmImmunologyBenzamidesCancer researchDisease ProgressionImatinib MesylateNeoplastic Stem CellsBone marrowbusinessBlood
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Inhibition of myosin light chain kinase reduces brain edema formation after traumatic brain injury.

2010

The role of the endothelial contractile apparatus in the process of brain edema formation after brain trauma is not characterized. Phosphorylation of myosin light chains by myosin light chain kinases (MLCK) activates endothelial contractile elements and results in a rearrangement of the cytoskeleton. This may enhance post-traumatic blood-brain barrier dysfunction. In order to investigate the role of the MLCK on brain edema formation and blood-brain barrier permeability after brain injury, mice were anesthetized and subjected to a controlled cortical impact (CCI). MLCK expression is significantly up-regulated after CCI with a maximum 12 h post-injury. Specific inhibition of MLCK by ML-7 resu…

MaleMyosin light-chain kinaseMyosin Light ChainsTime FactorsEndotheliumIntracranial PressureTraumatic brain injuryCentral nervous systemBrain Edemamacromolecular substancesBrain damageNaphthalenesBlood–brain barrierBiochemistryNeuroprotectionDrug Administration ScheduleFunctional LateralityStatistics NonparametricCerebral edemaCellular and Molecular NeuroscienceMicemedicineAnimalsEnzyme InhibitorsMyosin-Light-Chain KinaseNeurologic Examinationbusiness.industryAzepinesmedicine.diseaseConstrictionCell biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureGene Expression RegulationBlood-Brain BarrierBrain Injuriesmedicine.symptombusinessNeuroscienceEvans BlueJournal of neurochemistry
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Intensity of GABA-evoked responses is modified by nitric oxide-active compounds in the subthalamic nucleus of the rat: a microiontophoretic study.

2009

We have previously described modulatory effects of nitric oxide (NO)-active drugs on subthalamic nucleus (STN) neurons. In this study, the effects of microiontophoretically applied NO-active compounds on GABA-evoked responses were investigated in subthalamic neurons extracellularly recorded from anesthetized rats: 45 of 62 cells were excited by S-nitroso-glutathione (SNOG), an NO donor, whereas 28 of 43 neurons were inhibited by N-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor. Nearly all neurons responding to SNOG and/or L-NAME showed significant inhibitory responses to the administration of iontophoretic GABA. In these cells, the changes induced by NO-active drugs in the magnitud…

MaleNOS inhibitormedicine.drug_classBiophysicsAction PotentialsGlutamic AcidPharmacologyNeurotransmissionInhibitory postsynaptic potentialBicucullineNitric OxideSettore BIO/09 - FisiologiaNitric oxideGABA AntagonistsCellular and Molecular Neurosciencechemistry.chemical_compoundSubthalamic NucleusmedicineAnimalsDrug InteractionsNitric Oxide DonorsEnzyme InhibitorsRats Wistargamma-Aminobutyric AcidNeuronssubthalamic nucleus GABA SNOG L-NAMEIontophoresisBicucullineIontophoresisReceptor antagonistElectric StimulationRatsSubthalamic nucleusNG-Nitroarginine Methyl Esternervous systemchemistryS-Nitrosoglutathionemedicine.drugJournal of neuroscience research
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Catalase-independent early-gene expression in rat brain following acute ethanol exposure

2004

Early-gene expression evoked by acute ethanol treatment was studied in rat brain by quantitative immunocytochemistry, with reference to ethanol metabolism by the enzyme catalase. Colocalization with mu-opioid receptor (MOR) sites was also examined. Ethanol challenges [1, 2.5, and 4 g/kg intraperitoneally (i.p.)] evoked dose-dependent increases in c-Fos expression in several brain regions, but overlap with MOR-rich sites was only partial. Strong inhibition of brain catalase activity (ca. 60%) with 3-amino-1,2,4-triazole (AT, 1 g/kg i.p.) did not alter ethanol-induced c-Fos nor Krox-24 expression in any of the brain regions analyzed. This evidence demonstrates that catalase-mediated metabolis…

MaleNervous systemmedicine.medical_specialtyCentral nervous systemReceptors Opioid muGene ExpressionCell Countc-FosRats Sprague-DawleyInternal medicinemedicineAnimalsEnzyme InhibitorsEthanol metabolismMolecular BiologyAmitroleBrain ChemistryEthanolbiologyGeneral NeuroscienceBrainCentral Nervous System DepressantsColocalizationCatalaseImmunohistochemistryRatsmedicine.anatomical_structureEndocrinologyCatalasebiology.proteinNeurology (clinical)μ-opioid receptorProto-Oncogene Proteins c-fosImmediate early geneDevelopmental BiologyBrain Research
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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
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Critical role of nitric oxide on nicotine-induced hyperactivation of dopaminergic nigrostriatal system: electrophysiological and neurochemical eviden…

2010

Nicotine, the main psychoactive ingredient in tobacco, stimulates dopamine (DA) function, increasing DA neuronal activity and DA release. DA is involved in both motor control and in the rewarding and reinforcing effects of nicotine; however, the complete understanding of its molecular mechanisms is yet to be attained. Substantial evidence indicates that the reinforcing properties of drugs of abuse, including nicotine, can be affected by the nitric oxide (NO) system, which may act by modulating central dopaminergic function. In this study, using single cell recordings in vivo coupled with microiontophoresis and microdialysis in freely moving animals, the role of NO signaling on the hyperacti…

MaleNicotineIndazolesTime FactorsDopamineMicrodialysisAction PotentialsArginineSettore BIO/09 - FisiologiaCorpus striatumRats Sprague-DawleyAnimalsDrug InteractionsNicotinic Agonistsnigrostriatal systemEnzyme InhibitorsNeuronsAnalysis of VarianceDose-Response Relationship DrugResearchNitric oxideSubstantia NigraratsNG-Nitroarginine Methyl Esternervous system34-Dihydroxyphenylacetic Aciddopamine
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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
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Spontaneous mechanical activity and evoked responses in isolated gastric preparations from normal and dystrophic (mdx) mice

2002

This study examined whether alterations of the spontaneous and evoked mechanical activity are present in the stomach of the mdx mouse, the animal model for Duchenne muscular dystrophy. The gastric mechanical activity from whole-organ of normal and mdx mice was recorded in vitro as changes of intraluminal pressure. All gastric preparations developed spontaneous tone and phasic contractions, although the tone of the mdx preparations was significantly greater. Atropine reduced the tone of the two preparations by the same degree. Nomega-nitro-l-arginine methyl ester (l-NAME) significantly increased the tone and spontaneous contractions only in the stomach from normal animals, but did not affect…

MaleNitroprussideDuchenne muscular dystrophymedicine.medical_specialtymdx mouseContraction (grammar)PhysiologyDuchenne muscular dystrophyTetrodotoxinCholinergic AgonistsSettore BIO/09 - FisiologiaContractilityMicechemistry.chemical_compoundOrgan Culture TechniquesInternal medicinemedicineAnimalsNitric Oxide Donorsmdx mouseAnesthetics LocalEnzyme InhibitorsNeuroscience (all)Endocrine and Autonomic SystemsChemistryStomachStomachGastroenterologyMuscle SmoothNitric oxideAnatomyMuscular Dystrophy AnimalGastric smooth musclemedicine.diseaseElectric StimulationMuscular Dystrophy DuchenneGastric mechanical activityAtropineNG-Nitroarginine Methyl Estermedicine.anatomical_structureEndocrinologyMice Inbred mdxTetrodotoxinCholinergicCarbacholMuscle Contractionmedicine.drug
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