Search results for "NADP"

showing 10 items of 242 documents

Nitric oxide synthase in the enteric nervous system of the guinea-pig: a quantitative description

1994

The distribution and abundance of nitric oxide synthase (NOS)-containing neurons and their terminals in the gastrointestinal tract of the guinea-pig were examined in detail using NADPH diaphorase histochemistry and NOS immunohistochemistry. NOS-containing cell bodies were found in the myenteric plexus throughout the gastrointestinal tract and in the submucous plexus of the stomach, colon and rectum. NOS-containing neurons comprised between 12% (in the duodenum) and 54% (in the esophagus) of total myenteric neurons. In the ileum, NOS neurons represented 19% of total myenteric neurons. Most of the NOS neurons throughout the gastrointestinal tract possessed lamellar dendrites and a single axon…

Pathologymedicine.medical_specialtyHistologyMuscularis mucosaeColonDuodenumGuinea PigsMyenteric PlexusIleumBiologydigestive systemPathology and Forensic MedicineEsophagusNerve FibersIleummedicineSubmucous plexusAnimalsLarge intestineIntestinal MucosaMyenteric plexusNerve EndingsNeuronsHistocytochemistryStomachStomachdigestive oral and skin physiologyNADPH DehydrogenaseMuscle SmoothCell BiologyAnatomyImmunohistochemistrydigestive system diseasesmedicine.anatomical_structurenervous systemGastric MucosaBasal electrical rhythmEnteric nervous systemAmino Acid OxidoreductasesNitric Oxide SynthaseCell and Tissue Research
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Therapeutic effect of enhancing endothelial nitric oxide synthase (eNOS) expression and preventing eNOS uncoupling

2011

Nitric oxide (NO) produced by the endothelium is an important protective molecule in the vasculature. It is generated by the enzyme endothelial NO synthase (eNOS). Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain. Here, the substrate L-arginine is oxidized to L-citrulline and NO. Cardiovascular risk factors such as diabetes mellitus, hypertension, hypercholesterolaemia or cigarette smoking reduce bioactive NO. These risk factors lead to an enhanced productio…

PharmacologyFlavin adenine dinucleotideNADPH oxidasebiologyNitric Oxide Synthase Type IIIbiology.organism_classificationCofactorNitric oxidechemistry.chemical_compoundBiochemistrychemistryEnosbiology.proteinPeroxynitriteNicotinamide adenine dinucleotide phosphateBritish Journal of Pharmacology
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Molecular Mechanisms of the Crosstalk Between Mitochondrial and NADPH Oxidase Derived Reactive Oxygen Species in White Blood Cells - Implications for…

2012

Pharmacologychemistry.chemical_classificationCrosstalk (biology)Reactive oxygen speciesNADPH oxidasebiologyBiochemistrychemistryPhysiologybiology.proteinMolecular MedicineCell biology
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Molecular Mechanisms of the Crosstalk Between Mitochondria and NADPH Oxidase Through Reactive Oxygen Species—Studies in White Blood Cells and in Anim…

2014

Aims: Oxidative stress is involved in the development of cardiovascular disease. There is a growing body of evidence for a crosstalk between different enzymatic sources of oxidative stress. With the present study, we sought to determine the underlying crosstalk mechanisms, the role of the mitochondrial permeability transition pore (mPTP), and its link to endothelial dysfunction. Results: NADPH oxidase (Nox) activation (oxidative burst and translocation of cytosolic Nox subunits) was observed in response to mitochondrial reactive oxygen species (mtROS) formation in human leukocytes. In vitro, mtROS-induced Nox activation was prevented by inhibitors of the mPTP, protein kinase C, tyrosine kin…

PhysiologyNeutrophilsClinical BiochemistryBiologyMitochondrionmedicine.disease_causeBiochemistryModels BiologicalSuperoxide dismutaseCyclophilinsMiceForum Original Research CommunicationsMitochondria (A. Daiber Ed.)medicineLeukocytesAnimalsHumansMolecular BiologyGeneral Environmental ScienceRespiratory Burstchemistry.chemical_classificationMice KnockoutReactive oxygen speciesNADPH oxidaseSuperoxide DismutaseAngiotensin IINADPH OxidasesBiological TransportCell BiologyRespiratory burstMitochondriaPeroxidesEnzyme ActivationCrosstalk (biology)Oxidative StressMitochondrial permeability transition poreBiochemistrychemistrybiology.proteincardiovascular systemGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidation-ReductionOxidative stressCyclophilin D
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Reactive oxygen and ethylene are involved in the regulation of regurgitant-induced responses in bean plants.

2004

Summary Application of regurgitant from Leptinotarsa decemlineata Say on wound surfaces of one wounded leaf of intact bean ( Phaseolus vulgaris L.) plants resulted in activation of ethylene biosynthesis followed by an increase of both peroxidase and polyphenol oxidase activity. The aim of the present investigation was to study the source of increased oxidative enzyme activities in regurgitant-treated bean leaves and to determine if hydrogen peroxide and ethylene biosynthesis is responsible for regurgitant-induced amplification of wound responses in bean plants. As the regurgitant contained relative high activities of both peroxidase and polyphenol oxidase, there is a possibility that increa…

PhysiologyPlant SciencePolyphenol oxidaseSuperoxide dismutasechemistry.chemical_compoundPlant Growth RegulatorsOxidative enzymeAnimalsCycloheximideCatechol oxidasePlant DiseasesPhaseolusOxidase testNADPH oxidasebiologyTissue ExtractsImidazolesfood and beveragesAminooxyacetic AcidEthylenesAminooxyacetic acidColeopteraKineticschemistryBiochemistryPeroxidasesbiology.proteinReactive Oxygen SpeciesAgronomy and Crop ScienceCatechol OxidasePeroxidaseJournal of plant physiology
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Explaining the phenomenon of nitrate tolerance.

2005

During the last century, nitroglycerin has been the most commonly used antiischemic and antianginal agent. Unfortunately, after continuous application, its therapeutic efficacy rapidly vanishes. Neurohormonal activation of vasoconstrictor signals and intravascular volume expansion constitute early counter-regulatory responses (pseudotolerance), whereas long-term treatment induces intrinsic vascular changes, eg, a loss of nitrovasodilator-responsiveness (vascular tolerance). This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase …

PhysiologyVasodilator AgentsPharmacologymedicine.disease_causeNitric OxideProstacyclin synthaseNitric oxidechemistry.chemical_compoundNitroglycerinSuperoxidesPeroxynitrous AcidmedicineCyclic GMP-Dependent Protein KinasesAnimalsHumansBiotransformationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyChemistrySuperoxidePhosphoric Diester HydrolasesAldehyde Dehydrogenase MitochondrialDrug ToleranceAldehyde DehydrogenaseCyclic Nucleotide Phosphodiesterases Type 1VasodilationOxidative StressBiochemistryVasoconstrictioncardiovascular systembiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseReactive Oxygen SpeciesPeroxynitriteOxidative stressSignal TransductionCirculation research
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Regulation of NADPH oxidase-mediated superoxide production by acetylation and deacetylation

2021

Oral treatment of apolipoprotein E-knockout (ApoE-KO) mice with the putative sirtuin 1 (SIRT1) activator resveratrol led to a reduction of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity in the heart. In contrast, the SIRT1 inhibitor EX527 enhanced the superoxide production in isolated human polymorphonuclear granulocytes. In human monocytic THP-1 cells, phorbol ester-stimulated superoxide production was enhanced by inhibitors of histone deacetylases (HDACs; including quisinostat, trichostatin A (TSA), PCI34051, and tubastatin A) and decreased by inhibitors of histone acetyltransferases [such as garcinol, curcumin, and histone acetyltransferase (HAT) Inhibitor II]. Thes…

Physiologyresveratrolsirtuin 1histone acetyltransferaseSirtuinechemistry.chemical_compoundHistone deacetylasesSirtuin 1Physiology (medical)NADPH-OxidasemedicineQP1-981ddc:610Original ResearchacetylationAcetyltransferasenNADPH oxidasebiologyNADPH oxidaseSirtuin 1SuperoxideAcetylationHistone acetyltransferaseTrichostatin AchemistryBiochemistryHistone acetyltransferasesAcetylationResveratrolNADPH oxidaseshistone deacetylasebiology.proteinHistone deacetylaseDDC 610 / Medicine & healthNicotinamide adenine dinucleotide phosphateRac1medicine.drug
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Protective effect of apocynin in a mouse model of chemically-induced colitis.

2013

Apocynin, a constituent of Picrorhiza kurroa, successfully inhibits NADPH oxidase and shows promise as an anti-inflammatory drug. Now, we report anti-inflammatory effects of apocynin in an experimental colitis model induced by dextran sulfate sodium as well as the effects on the mediators involved in this process. Apocynin reduced the colitis induced in mice by administration of 5 % dextran sulfate sodium during 7 days. Mice were fed a control diet or a diet supplemented with 2 % of apocynin or 2 % of rutin. Sulfasalazine (50 mg/kg, p. o.) was used as a positive control. Treatment with apocynin and rutin ameliorated the course of colonic inflammation with results similar to those of the ref…

Picrorhiza kurroaRutinAnti-Inflammatory AgentsPharmaceutical ScienceNitric Oxide Synthase Type IIPharmacologyInflammatory bowel diseaseAnalytical Chemistrychemistry.chemical_compoundRutinMiceDrug DiscoveryPicrorhizaNADPH oxidasebiologyDextran SulfateColitisBiochemistrycardiovascular systemMolecular Medicinecirculatory and respiratory physiologymedicine.druginorganic chemicalsSTAT3 Transcription FactorColonNitric OxideDinoprostoneNitric oxideSulfasalazinemedicineAnimalscardiovascular diseasesColitisPharmacologyCyclooxygenase 2 Inhibitorsbusiness.industryPlant ExtractsOrganic ChemistryTranscription Factor RelAAcetophenonesmedicine.diseaseSulfasalazineDisease Models AnimalchemistryComplementary and alternative medicineCyclooxygenase 2Apocyninbiology.proteinbusinessPhytotherapyPlanta medica
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Antitumor effects of dehydroxymethylepoxyquinomicin, a novel nuclear factor-kappaB inhibitor, in human liver cancer cells are mediated through a reac…

2009

Activation of the nuclear transcription factor-kappa B (NF-kappa B) has been implicated in liver tumorigenesis. We evaluated the effects of a novel NF-kappa B inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), in two human liver cancer cell lines HA22T/VGH and HuH-6. DHMEQ treatment dose dependently decreased the DNA-binding capacity of the NF-kappa B p65 subunit, inhibited cell growth and proliferation, and increased apoptosis as shown by caspase activation, release of cytochrome c, poly(ADP-ribose) polymerase cleavage, and down-regulation of survivin. DHMEQ also induced a dose-dependent activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling, …

Programmed cell deathCarcinoma HepatocellularBIOLOGICAL-ACTIVITIESDrug Evaluation PreclinicalDown-RegulationAntineoplastic AgentsApoptosisBiologymedicine.disease_causeACTIVATIONchemistry.chemical_compoundHYDROGEN-PEROXIDEENDOPLASMIC-RETICULUM STRESSCell Line TumorSurvivinNADPH OXIDASEmedicineHumansOXIDATIVE STRESSProtein kinase AEndoplasmic Reticulum Chaperone BiPINDUCED APOPTOSISCell ProliferationPharmacologySettore MED/12 - GastroenterologiaDose-Response Relationship DrugUNFOLDED PROTEIN RESPONSECell growthCyclohexanonesINDUCTIONLiver NeoplasmsDEATHNF-kappa BCytochromes cMolecular biologyCell biologyEnzyme ActivationchemistryApoptosisCaspasesCancer cellBenzamidesSettore BIO/14 - FarmacologiaMolecular MedicineGrowth inhibitionMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesOxidative stressMolecular pharmacology
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Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
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