Search results for " Type II"

showing 10 items of 542 documents

iNOS-derived nitric oxide mediates the increase in TFF2 expression associated with gastric damage: role of HIF-1.

2009

Trefoil (TFF) peptides are involved in gastrointestinal mucosal restitution. An hypoxia inducible factor 1 (HIF-1)-dependent induction of TFF genes has been reported in gastric epithelial cells. Nitric oxide (NO) is associated with mucosal damage and modulates HIF-1 activity. The aim of the present study was to analyze the role of iNOS-derived NO in HIF-1alpha stabilization and TFF gene expression in damaged gastric mucosa. Aspirin caused gastric injury that peaked 6 h after dosing and returned to normality at 24 h. iNOS mRNA expression occurs in the corpus in parallel with damage. Blockade of iNOS activity did not modify gastric lesions induced by aspirin but delayed mucosal healing. Aspir…

MaleBenzylaminesAmidinesNitric Oxide Synthase Type IINitric OxideBiochemistryNitric oxideCell LineRats Sprague-Dawleychemistry.chemical_compoundMiceDownregulation and upregulationGene expressionGeneticsGastric mucosamedicineGene silencingAnimalsHumansRNA MessengerEnzyme InhibitorseducationMolecular BiologyDNA Primerseducation.field_of_studyWound HealingAspirinBase SequenceAnti-Inflammatory Agents Non-SteroidalTrefoil factor 2Macrophage ActivationHypoxia-Inducible Factor 1 alpha SubunitCoculture TechniquesRatsUp-RegulationMicroRNAsmedicine.anatomical_structurechemistryCell cultureGastric MucosaCancer researchTrefoil Factor-2Wound healingPeptidesBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Inhibition of iNOS activity by 1400W decreases glutamate release and ameliorates stroke outcome after experimental ischemia

2005

Background and purpose. It has been shown that the reversed operation of glutamate transporters when ATP levels fall accounts for most glutamate release induced by severe cerebral ischemia. Nitric oxide (NO) is formed after ischemia and causes ATP depletion. Our purpose is to test if NO release from inducible NO synthase (iNOS) after stroke may cause a delayed glutamate release due to ATP depletion that might underlie progression of the ischemic infarct. We have studied the effect of the highly selective inhibitor of iNOS activity 1400W on brain ATP levels, extracellular glutamate, and stroke outcome after transient focal cerebral ischemia in rats. Methods. To induce focal ischemia, the mid…

MaleBenzylaminesAmino Acid Transport System X-AGIschemiaAmidinesInfarctionDown-RegulationGlutamic AcidNitric Oxide Synthase Type IIL-argininePharmacologyNeuroprotectionNitric oxidelcsh:RC321-571chemistry.chemical_compoundAdenosine TriphosphateWestern blotmedicine.arteryStroke outcomeMedicineAnimalscardiovascular diseasesEnzyme InhibitorsRats Wistarlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymedicine.diagnostic_testbusiness.industryGlutamate receptorBrainInfarction Middle Cerebral ArteryNitric oxideCerebral Infarctionmedicine.diseaseNeuroprotectionRatsATPStrokeDisease Models AnimalNeuroprotective AgentsTreatment OutcomeNeurologychemistryCytoprotectionIschemic Attack TransientAnesthesiaMiddle cerebral arteryNitric Oxide SynthaseGlutamatebusinessNeurobiology of Disease
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Effect of autologous blood transfusion on cerebral cytokine expression.

2011

BACKGROUND: Autologous blood transfusion (ABT), for example, by means of cell saver equipment, is used to reduce the need for allogenic blood transfusion in patients with high perioperative blood loss. This study investigated the effect of blood/extracorporal surface interaction during withdrawal and retransfusion of shed autologous blood on cerebral inflammation in rats. Rats subjected to hypotension with cerebral ischemia served as positive controls. METHODS: Eighty-eight male Sprague-Dawley rats were anesthetized with sevoflurane, instrumented, and randomly assigned to the following groups: sham-operation (SHAM), autologous blood withdrawal/transfusion only (ABT), or bilateral carotid ar…

MaleBlood transfusionmedicine.medical_treatmentInterleukin-1betaIschemiaNitric Oxide Synthase Type IIInflammationPharmacologySevofluraneRats Sprague-DawleyBlood Transfusion AutologousmedicineHippocampus (mythology)AnimalsInterleukin 6biologybusiness.industryInterleukin-6Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaBrainmedicine.diseaseRatsNitric oxide synthaseAnesthesiology and Pain MedicineCyclooxygenase 2biology.proteinCytokinesSurgeryTumor necrosis factor alphaNeurology (clinical)medicine.symptombusinessmedicine.drugFollow-Up StudiesJournal of neurosurgical anesthesiology
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Phytochemical and pharmacological studies on the acetonic extract of Marrubium globosum ssp. libanoticum

2006

A new natural labdane diterpene, marrulibanoside, was isolated from the acetonic extract of aerial parts of M. globosum Montbr. et Auch. ex Benth. ssp. libanoticum Boiss. (Lamiaceae). Its structure was determined by spectroscopic methods such as 1D and 2D NMR and mass spectrometry. Pharmacological studies have shown that the extract of M. globosum exerts anti-inflammatory effects in the rat paw oedema induced by carrageenin resulting in reduced paw swelling. This activity, which seems due to marrulibanoside, is a consequence of iNOS and COX-2 activities inhibition.

MaleBlotting WesternPharmaceutical ScienceNitric Oxide Synthase Type IIPharmacognosyLABDANE DITERPENOIDSCarrageenanDinoprostoneAnalytical Chemistrylaw.inventionLabdanechemistry.chemical_compoundMicelawDrug DiscoveryBotanyVULGAREAnimalsEdemaRats WistarPharmacologybiologyTraditional medicinePlant ExtractsOrganic ChemistryAnti-Inflammatory Agents Non-SteroidalCYLLENEUMPlant Components Aerialbiology.organism_classificationCarrageenanRatsComplementary and alternative medicinechemistryPhytochemicalMacrophages PeritonealMolecular MedicineLamiaceaeVELUTINUMDiterpenePhytotherapyMarrubiumMarrubiumPhytotherapy
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Role of endothelial nitric oxide in pulmonary and systemic arteries during hypoxia

2014

Abstract Our aim was to investigate the role played by endothelial nitric oxide (NO) during acute vascular response to hypoxia, as a modulator of both vascular tone (through guanylate cyclase (sGC) activation) and mitochondrial O2 consumption (through competitive inhibition of cytochrome-c-oxydase (CcO)). Organ bath experiments were performed and O2 consumption (Clark electrode) was determined in isolated aorta, mesenteric and pulmonary arteries of rats and eNOS-knockout mice. All pre-contracted vessels exhibited a triphasic hypoxic response consisting of an initial transient contraction (not observed in vessels from eNOS-knockout mice) followed by relaxation and subsequent sustained contra…

MaleCancer ResearchContraction (grammar)Nitric Oxide Synthase Type IIIEndotheliumPhysiologyClinical BiochemistryVasodilationPulmonary ArteryMitochondrionPharmacologyNitric OxideBiochemistryNitric oxideRats Sprague-DawleyMicechemistry.chemical_compoundNon-competitive inhibitionEnosmedicineAnimalsHypoxiaAortaMice KnockoutbiologyMyxothiazolEndothelial Cellsbiology.organism_classificationMesenteric ArteriesRatsMice Inbred C57BLmedicine.anatomical_structurechemistryAnesthesiacardiovascular systemNitric Oxide
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Midostaurin upregulates eNOS gene expression and preserves eNOS function in the microcirculation of the mouse

2005

Nitric oxide (NO) derived from endothelial NO synthase (eNOS) is a powerful vasodilator and possesses vasoprotective effects. Therefore, augmentation of eNOS expression and -activity by pharmacological means could provide protection against cardiovascular disease. However, this concept has been questioned recently, because in several disease models, eNOS upregulation was associated with a dysfunctional enzyme (referred to as eNOS uncoupling). In contrast, the present study demonstrates that an eNOS gene expression-enhancing compound with additional protein kinase C (PKC) inhibitory properties can upregulate eNOS while preserving its enzymatic function. Apolipoprotein E-knockout mice were tr…

MaleCancer ResearchNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryNitric Oxide Synthase Type IIBiologyPharmacologyBiochemistryNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosmedicineAnimalsStaurosporineRNA MessengerMidostaurinAortaNitritesProtein kinase CMice KnockoutNitratesMicrocirculationStaurosporinebiology.organism_classificationVasoprotectiveVasodilationNitric oxide synthaseBiochemistrychemistryEnzyme Inductionbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesIntravital microscopymedicine.drugNitric Oxide
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Oncogene-driven intrinsic inflammation induces leukocyte production of tumor necrosis factor that critically contributes to mammary carcinogenesis.

2010

Abstract Oncogene activation promotes an intrinsic inflammatory pathway that is crucial for cancer development. Here, we have investigated the actual effect of the inflammatory cytokine tumor necrosis factor (TNF) on the natural history of spontaneous mammary cancer in the HER2/neuT (NeuT) transgenic mouse model. Bone marrow transplantation from TNF knockout mice into NeuT recipients significantly impaired tumor growth, indicating that the source of TNF fostering tumor development was of bone marrow origin. We show that the absence of leukocyte-derived TNF disarranged the tumor vasculature, which lacked pericyte coverage and structural integrity, leading to diffuse vascular hemorrhage and s…

MaleCancer ResearchStromal cellmedicine.medical_treatmentInflammationmedicine.disease_causeAntibodiesArticleMicemedicineLeukocytesAnimalsHumansReceptors Tumor Necrosis Factor Type IItumor necrosis factor mammary carcinogenesis.Crosses GeneticBone Marrow TransplantationInflammationMice KnockoutOncogenebusiness.industryTumor Necrosis Factor-alphaCancerMammary Neoplasms ExperimentalOncogenesmedicine.diseaseImmunohistochemistryMice Inbred C57BLPlatelet Endothelial Cell Adhesion Molecule-1medicine.anatomical_structureCytokineOncologyReceptors Tumor Necrosis Factor Type IImmunologyTumor necrosis factor alphaFemaleBone marrowmedicine.symptomCarcinogenesisbusinessCancer research
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Nitric oxide-mediated inhibition of androgen receptor activity: possible implications for prostate cancer progression.

2006

Chronic inflammation increases the risk of cancer and many cancers, including prostate cancer, arise at sites of chronic inflammation. Inducible nitric oxide synthase (iNOS) is an enzyme dominantly expressed during inflammatory reactions. Although synthesis of high amounts of nitric oxide (NO) by iNOS has been demonstrated in pathophysiological processes, such as acute or chronic inflammation, autoimmune diseases or tumorigenesis, the role of iNOS activity in most of these diseases is poorly understood. Analysing prostate cancer biopsies by immunohistochemistry we found iNOS protein expression in tumor cells strongly paralleled by nitrotyrosine suggesting that iNOS is fully active. In vitro…

MaleCancer Researchmedicine.medical_specialtymedicine.drug_classNitric Oxide Synthase Type IIBiologymedicine.disease_causeNitric OxideProstate cancerProstateInternal medicineCell Line TumorGeneticsmedicineAndrogen Receptor AntagonistsHumansAndrogen Receptor AntagonistsMolecular BiologyReverse Transcriptase Polymerase Chain ReactionCancerProstatic NeoplasmsAndrogenmedicine.diseaseImmunohistochemistryAndrogen receptormedicine.anatomical_structureEndocrinologyTumor progressionReceptors AndrogenDisease ProgressionCarcinogenesisOncogene
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Gene therapy with iNOS enhances regional contractility and reduces delayed contrast enhancement in a model of postischemic congestive heart failure

2012

Aims: The purpose of this study was to evaluate the effect of transient local myocardial gene transfer of iNOS on cardiac function in a large mammal animal model of heart failure induced by chronic ischemia. Methods: Chronic myocardial ischemia was induced using a minimally invasive model in 16 landrace pigs. Upon demonstration of heart failure, eight animals were treated with liposome-mediated iNOS-gene-transfer by local intramyocardial injection; eight animals received a sham procedure to serve as control. Results: The transmurality of late enhancement (control: 46.4%, iNOS: 35.9%; p < 0.05) was significantly decreased in the ischemic area in the iNOS-treated group. Wall thickness at end-…

MaleCardiac function curvemedicine.medical_specialtyTiclopidineSwinePhysiologySus scrofaMyocardial IschemiaIschemiaContrast MediaNitric Oxide Synthase Type IIGadoliniumCoronary AngiographyContractilityRandom AllocationVentricular Dysfunction LeftGenes ReporterFibrosisPhysiology (medical)Internal medicineGenes SyntheticmedicineAnimalsTiclopidineHeart FailureDrug CarriersAspirinAspirinmedicine.diagnostic_testbusiness.industryCoronary StenosisAnticoagulantsMagnetic resonance imagingGenetic TherapyHematologymedicine.diseaseFibrosisMagnetic Resonance ImagingMyocardial ContractionClopidogrelDisease Models AnimalHeart failureLiposomesCardiologyFemaleStentsCardiology and Cardiovascular Medicinebusinessmedicine.drugClinical Hemorheology and Microcirculation
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Neuroprotective properties of mildronate, a mitochondria-targeted small molecule.

2010

Mildronate, a representative of the aza-butyrobetaine class of drugs with proven cardioprotective efficacy, was recently found to prevent dysfunction of complex I in rat liver mitochondria. The present study demonstrates that mildronate also acts as a neuroprotective agent. In a mouse model of azidothymidine (anti-HIV drug) neurotoxicity, mildronate reduced the azidothymidine-induced alterations in mouse brain tissue: it normalized the increase in caspase-3, cellular apoptosis susceptibility protein (CAS) and iNOS expression assessed by quantitative and semi-quantitative analysis. Mildronate also normalized the changes in cytochrome c oxidase (COX) expression, reduced the expression of glia…

MaleCell signalingAnti-HIV AgentsNitric Oxide Synthase Type IIMice Inbred StrainsMitochondrionPharmacologyNeuroprotectionElectron Transport Complex IVMiceCellular Apoptosis Susceptibility ProteinGlial Fibrillary Acidic ProteinmedicineAnimalsLymphocytesNeuroinflammationGlial fibrillary acidic proteinbiologyCaspase 3General NeuroscienceNeurodegenerationNeurotoxicityBrainmedicine.diseaseDisease Models AnimalNeuroprotective AgentsBiochemistrybiology.proteinNeurotoxicity SyndromesZidovudineCellular apoptosis susceptibility proteinMethylhydrazinesNeuroscience letters
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