Search results for "enzyme inhibitors"

showing 10 items of 559 documents

Mechanisms underlying the inhibitory effects induced by pituitary adenylate cyclase-activating peptide in mouse ileum

2005

Abstract The aim of this study was to investigate the signal transduction mechanisms underlying the inhibitory effect induced by pituitary adenylate cyclase activating peptide (PACAP-27) on the spontaneous contractile activity of longitudinal muscle of mouse ileum. Mechanical activity of ileal segments was recorded isometrically in vitro. PACAP-27 produced apamin-sensitive reduction of the amplitude of the spontaneous contractions. 9-(Tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), adenylate cyclase inhibitor, or genistein and tyrphostin 25, tyrosine kinase inhibitors, had negligible effects on PACAP-27-induced inhibition. PACAP-27 effects were significantly inhibited by U-73122, phopho…

MaleIndolesPhosphodiesterase InhibitorsVasodilator AgentsMouse ileumStimulationSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundInositolEnzyme InhibitorsEstrenesRyanodineRyanodine receptorProtein-Tyrosine KinasesTyrphostinsGenisteinPyrrolidinonesCell biologyPituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterPituitary Adenylate Cyclase-Activating PolypeptideThapsigarginSignal transductionCyclopiazonic acidhormones hormone substitutes and hormone antagonistsMuscle ContractionBoron Compoundsendocrine systemmedicine.medical_specialtyThapsigarginMuscular inhibitionCalcium-Transporting ATPasesIn Vitro TechniquesInositol 145-triphosphateBiologyPACAP-27 (pituitary adenylate cyclase activating peptide)IleumPhospholipase CInternal medicinemedicineAnimalsPharmacologyDose-Response Relationship DrugPhospholipase CAdenineMuscle SmoothMice Inbred C57BLEndocrinologyApaminchemistryAdenylyl Cyclase InhibitorsCalciumNitric Oxide SynthaseEuropean Journal of Pharmacology
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The ineffectiveness of the NO-cyclic GMP signaling pathway in the atrial myocardium

1995

1. This study was performed to determine whether nitric oxide (NO) has direct effects on force of contraction (Fc) in atrial myocardium from rats, rabbits, guinea-pigs, frogs, and man. 2. Glyceryl trinitrate, isosorbide dinitrate, 3-morpholino-sydnonimine hydrochloride (SIN-1), and S-nitroso-N-acetylpenicillamine (SNAP) did not significantly reduce Fc in the various preparations investigated, either given alone or after stimulation of alpha- or beta-adrenoceptors. 3. SNAP did not change the time course of contractions in rat, guinea-pig and human preparations. 4. 8-Bromo-guanosine-3':5'-cyclic monophosphate (8-Br-cyclic GMP) produced a negative inotropic effect in rat, guinea-pig and human …

MaleInotropemedicine.medical_specialtyContraction (grammar)RanidaeVasodilator AgentsGuinea PigsGuanosine MonophosphateArginineNitric OxideNitric oxideRats Sprague-DawleyContractilitychemistry.chemical_compoundInternal medicinemedicineAnimalsHumansHeart AtriaEnzyme InhibitorsPharmacologyomega-N-MethylargininebiologyChemistrySnapAtrial FunctionMyocardial ContractionAcetylcholineRatsNitric oxide synthaseEndocrinologybiology.proteinOmega-N-MethylarginineCarbacholFemaleRabbitsNitric Oxide SynthaseIsosorbide dinitrateSignal TransductionResearch Articlemedicine.drugBritish Journal of Pharmacology
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The cytotoxicity of mitomycin C and Adriamycin in genetically engineered V79 cell lines and freshly isolated rat hepatocytes

1995

The objective of the present study was to investigate the cytotoxicity of Adriamycin (ADR) and mitomycin C (MMC) in tumor and non-tumor cells with respect to the role of cytochrome P450 (P450). Therefore, genetically engineered V79 Chinese hamster fibroblasts expressing only single enzymes of P450 were used. SD1 and XEM2 cells expressed rat P450IIB1 and P450IA1, respectively, whereas the V79 parental cells contained no detectable P450 levels. The cytotoxicity of ADR and MMC in the V79 cell system was compared with that in freshly isolated hepatocytes from phenobarbital (PB-hepatocytes)- and beta-naphthoflavone (beta NF-hepatocytes)-induced rats. Following 24 h of exposure to ADR equal cytot…

MaleLiver cytologyMitomycinBiologyTransfectionToxicologyDihydroxydihydrobenzopyrenesCricetulusCytochrome P-450 Enzyme Systembeta-NaphthoflavoneSDG 3 - Good Health and Well-beingCricetinaemedicineAnimalsCytotoxic T cellEnzyme InhibitorsRats WistarCytotoxicityCyclophosphamideCells CulturedBenzoflavonesCell DeathL-Lactate DehydrogenaseMitomycin CMaleatesGeneral MedicineTransfectionFibroblastsMetyraponerespiratory systemMolecular biologyIn vitroRatsmedicine.anatomical_structureLiverBiochemistryDoxorubicinCell cultureEnzyme InductionPhenobarbitalHepatocyte/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingChemico-Biological Interactions
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Phosphorylation of extracellular signal-related protein kinase is required for rapid facilitation of heat-induced currents in rat dorsal root ganglio…

2005

A subgroup of dorsal root ganglion (DRG) neurons responds to noxious heat with an influx of cations carried by specific ion channels such as the transient receptor potential channel of the vanilloid receptor type, subtype 1 (TRPV1). Application of capsaicin induces a reversible facilitation of these currents. This facilitation could be an interaction of two agonists at their common receptor or be caused by an influx of calcium ions into the cell. Calcium influx into the cell can activate protein kinases such as the extracellular signal-related protein kinase (ERK) pathway. This study explored the kinetics, calcium-dependency and intracellular signals following application of capsaicin and l…

MaleMAPK/ERK pathwayHot TemperaturePatch-Clamp TechniquesStatistics as TopicTRPV1BiologyMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundBAPTAGanglia SpinalNitrilesButadienesAnimalsDrug InteractionsEnzyme InhibitorsPhosphorylationExtracellular Signal-Regulated MAP KinasesProtein kinase AProtein kinase CNeuronsAnalysis of VarianceDose-Response Relationship DrugGeneral NeuroscienceMEK inhibitorRatsCell biologychemistryBiochemistryCapsaicinMitogen-activated protein kinasebiology.proteinCalciumFemaleCapsaicinNeuroscience
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Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
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Long-Term Clinical Outcomes According to Previous Manifestations of Atherosclerotic Disease (from the FAST-MI 2010 Registry)

2017

IF 3.398; International audience; The prognosis of patients with acute myocardial infarction (AMI) has notably improved in the past 20 years. Using the French Registry of ST-Elevation and Non-ST-elevation Myocardial Infarction (FAST-MI) 2010 registry, we investigated whether previous manifestations of atherosclerotic disease (i.e., previous MI, or a history of any form of atherosclerotic disease) are at truly increased risk compared with those in whom AMI is the first manifestation of the disease. FAST-MI 2010 is a nationwide French registry including 3,079 patients with AMI, among whom 1,062 patients had a history of cardiovascular atherosclerotic disease and 498 patients had a history of …

MaleMESH : Atherosclerosismedicine.medical_treatmentMESH : MortalityMyocardial InfarctionMESH : AgedMESH : Prospective StudiesAngiotensin-Converting Enzyme InhibitorsCoronary Artery DiseaseDiseaseMESH : Cerebrovascular Disorders0302 clinical medicineMedicineLongitudinal StudiesProspective StudiesMESH: Coronary Artery DiseaseMyocardial infarctionCoronary Artery BypassMESH: Treatment OutcomeCause of deathAged 80 and overeducation.field_of_studyMESH: Middle AgedHazard ratioMESH : Platelet Aggregation InhibitorsPrognosisMESH: Case-Control Studies3. Good healthMESH: Myocardial InfarctionMESH: Angiotensin Receptor AntagonistsMESH : Angiotensin-Converting Enzyme InhibitorsCardiology and Cardiovascular MedicineMESH: Percutaneous Coronary InterventionMESH : Case-Control Studiesmedicine.medical_specialtyMESH : Angiotensin Receptor AntagonistsMESH: Prognosis03 medical and health sciencesPercutaneous Coronary Intervention[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemHumansMESH : Middle AgedMESH : Coronary Artery DiseaseMESH : Aged 80 and overMESH: Hydroxymethylglutaryl-CoA Reductase InhibitorseducationMESH: Age DistributionAgedMESH: HumansMESH: MortalityProportional hazards modelMESH: Coronary Artery BypassMESH : HumansCase-control studyMESH : Proportional Hazards Modelsmedicine.diseaseMESH : Coronary Artery BypassCase-Control StudiesMESH: FemaleMESH: RegistriesMESH : Age Distribution030204 cardiovascular system & hematologyMESH: AtherosclerosisMESH: Proportional Hazards ModelsMESH: Cause of DeathMESH: Aged 80 and overMESH : Percutaneous Coronary InterventionRisk FactorsMESH: Risk FactorsCause of DeathMESH : FemaleRegistries030212 general & internal medicineMESH: Longitudinal StudiesMESH : Longitudinal StudiesMESH: AgedMESH : PrognosisMESH: Angiotensin-Converting Enzyme InhibitorsMESH: Adrenergic beta-AntagonistsMiddle Aged[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMESH : Risk FactorsTreatment OutcomeMESH: Platelet Aggregation InhibitorsCardiologyFemaleMESH: Cerebrovascular DisordersFranceMESH : MaleAdrenergic beta-AntagonistsMESH : Adrenergic beta-AntagonistsPopulationMESH : Treatment OutcomeMESH: Multivariate AnalysisAngiotensin Receptor AntagonistsAge DistributionInternal medicineMortalityMESH : FranceProportional Hazards ModelsMESH : Cause of Deathbusiness.industryMESH : Hydroxymethylglutaryl-CoA Reductase InhibitorsMESH : Multivariate AnalysisPercutaneous coronary interventionAtherosclerosisMESH: MaleMESH: Prospective StudiesMESH: FranceCerebrovascular DisordersMultivariate AnalysisHydroxymethylglutaryl-CoA Reductase InhibitorsMESH : Myocardial InfarctionbusinessPlatelet Aggregation InhibitorsMESH : RegistriesThe American Journal of Cardiology
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Impact of 7-Ketocholesterol and Very Long Chain Fatty Acids on Oligodendrocyte Lipid Membrane Organization: Evaluation Via LAURDAN and FAMIS Spectral…

2011

International audience; In the context of multiple sclerosis and X-linked adrenoleukodystrophy, 7-ketocholesterol (7KC) and very long chain fatty acids (C24:0, C26:0) are supposed to induce side effects respectively on oligodendrocytes which are myelin (which is a lipoproteic complex) synthesizing cells. The effects of 7KC (25, 50 mu M), C24:0 and C26:0 (10, 20 mu M) on cell viability and lipid membrane organization were investigated on 158N murine oligodendrocytes. Concerning 7KC and fatty acids (at 20 mu M only):1) cell growth was strongly inhibited; 2) marked induction of cell death was revealed with propidium iodide (PI); 3) no apoptotic cells were found with C24:0 and C26:0 (absence of…

MaleMYELINlaw.inventionchemistry.chemical_compoundMice0302 clinical medicinelawFAMIS2-Naphthylamine[SDV.IDA]Life Sciences [q-bio]/Food engineeringEnzyme InhibitorsLipid bilayerKetocholesterols0303 health sciencesMicroscopy ConfocalOXYSTEROLSFatty AcidsMULTIPLE-SCLEROSISvery long chain fatty acidsCell biologyPEROXISOMAL DISORDERSAPOPTOSISOligodendrogliaX-LINKED ADRENOLEUKODYSTROPHYmedicine.anatomical_structureMembraneCHOLESTEROL OXIDESlipids (amino acids peptides and proteins)Laurdanalpha-CyclodextrinsHistologyContext (language use)BiologyMETABOLISMPathology and Forensic Medicine158N oligodendrocytes03 medical and health sciencesMembrane LipidsConfocal microscopymedicineAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringViability assayPropidium iodideLAURDAN7-ketocholesterol030304 developmental biologyFluorescent DyesCell MembraneCENTRAL-NERVOUS-SYSTEMCell BiologyOligodendrocytechemistryCELLSmono-photon confocal microscopy030217 neurology & neurosurgeryLaurates
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1-imidazolyl(alkyl)-substituted di- and tetrahydroquinolines and analogues: syntheses and evaluation of dual inhibitors of thromboxane A(2) synthase …

2000

A series of 1-imidazolyl(alkyl)-substituted quinoline, isoquinoline, naphthalene, benzo[b]furan, and benzo[b]thiophene derivatives was synthesized as dual inhibitors of thromboxane A(2) synthase (P450 TxA(2)) and aromatase (P450 arom). Dual inhibition of these enzymes could be a novel strategy for the treatment of mammary tumors and the prophylaxis of metastases. The most potent dual inhibitors, 5-(2-imidazol-1-ylethyl)-7,8-dihydroquinoline (31) (P450 TxA(2): IC(50) = 0.29 microM; P450 arom: IC(50) = 0.50 microM) and its 5, 6-saturated analogue 30 (P450 TxA(2): IC(50) = 0.68 microM; P450 arom: IC(50) = 0.38 microM), showed a stronger inhibition of both target enzymes than the reference comp…

MaleMagnetic Resonance SpectroscopyThromboxaneStereochemistryIn Vitro TechniquesSubstrate SpecificityRats Sprague-DawleyThromboxane A2chemistry.chemical_compoundLipoxygenaseThromboxane A2MicrosomesDrug DiscoveryAnimalsHumansDazoxibenIsoquinolineEnzyme InhibitorsbiologyAromatase InhibitorsImidazolesRatsThromboxane B2Thromboxane B2chemistrybiology.proteinQuinolinesMolecular MedicineSpectrophotometry UltravioletThromboxane-A synthaseCyclooxygenaseThromboxane-A SynthaseJournal of medicinal chemistry
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Zofenopril and ramipril in patients with left ventricular systolic dysfunction after acute myocardial infarction: A propensity analysis of the Surviv…

2016

Introduction: This was a propensity score analysis of the prospective, randomized, double-blind Survival of Myocardial Infarction Long-term Evaluation (SMILE) 4 study in which one-year treatment with zofenopril 60 mg plus acetylsalicylic acid (ASA) 100 mg gave superior results compared to ramipril 10 mg plus ASA in terms of death or hospitalization for cardiovascular causes in patients with acute myocardial infarction (AMI) complicated by left ventricular dysfunction (LVD). Materials and methods: A total of 716 patients of the intention-to-treat population were divided into homogeneous propensity quintiles (Q) using a logistic regression model (QI: best risk profile; QV: worst risk profile)…

MaleMedicine (General)Time FactorsCaptoprilIntention to Treat AnalysiLeftMyocardial Infarction030204 cardiovascular system & hematologychemistry.chemical_compoundVentricular Dysfunction Left0302 clinical medicineEndocrinologyRamiprilPropensity analysisAcetylsalicylic acid; Acute myocardial infarction; Angiotensin-converting enzyme inhibitors; Left ventricular dysfunction; Propensity analysis; Captopril; Demography; Drug Therapy Combination; Endpoint Determination; Female; Hospitalization; Humans; Intention to Treat Analysis; Male; Middle Aged; Myocardial Infarction; Ramipril; Survival Analysis; Time Factors; Ventricular Dysfunction Left; Propensity Score; Internal Medicine; EndocrinologyVentricular DysfunctionMedicine030212 general & internal medicineMyocardial infarctioneducation.field_of_studyLeft ventricular dysfunctionElectrocardiography in myocardial infarctionMiddle AgedZofenoprilIntention to Treat AnalysisHospitalizationCombinationCardiologyOriginal ArticleDrug Therapy CombinationFemaleSurvival AnalysiPropensity analysimedicine.drugHumanRamiprilmedicine.medical_specialtyTime FactorEndpoint DeterminationPopulationAcute myocardial infarction03 medical and health sciencesR5-920Drug TherapyInternal medicineAngiotensin-converting enzyme inhibitorsAcetylsalicylic acidInternal MedicineHumanseducationPropensity ScoreDemographybusiness.industryOdds ratiomedicine.diseaseSurvival AnalysisConfidence intervalchemistryAngiotensin-converting enzyme inhibitorPropensity score matchingbusiness
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7-nitroindazole protects striatal dopaminergic neurons against MPP+-induced degeneration: an in vivo microdialysis study.

2007

The neuropathological hallmark of Parkinson's disease (PD) is the selective degeneration of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNc). In this study, using a microdialysis technique, we investigated whether an inhibitor of neuronal nitric oxide synthase (nNOS), 7-nitrindazole (7-NI), could protect against DAergic neuronal damage induced by in vivo infusion of 1-methyl-4-phenylpiridinium iodide (MPP(+)) in freely moving rats. Experiments were performed over 2 days in three groups of rats: (a) nonlesioned, (b) MPP(+)-lesioned, and (c) 7-NI pretreated MPP(+)-lesioned rats. On day 1, control rats were perfused with an artificial CSF, while 1 mM MPP(+) was infuse…

MaleMicrodialysis1-Methyl-4-phenylpyridinium7-NitroindazoleIndazolesDopamineMicrodialysisSubstantia nigraStriatumNitric Oxide Synthase Type IPharmacologyNeuroprotectionGeneral Biochemistry Genetics and Molecular BiologyRats Sprague-Dawleychemistry.chemical_compoundHistory and Philosophy of SciencemedicineAnimalsEnzyme InhibitorsNeuronsPars compactaChemistryGeneral NeuroscienceDopaminergicNeurotoxicityParkinson Diseasemedicine.diseaseRatsSubstantia NigraDisease Models AnimalNeuroprotective Agentsnervous systemNeuroscienceAnnals of the New York Academy of Sciences
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