Search results for " Peritoneal"

showing 10 items of 87 documents

4-dimethylamino-3′,4′-dimethoxychalcone downregulates iNOS expression and exerts anti-inflammatory effects

2001

Abstract Reactive oxygen and nitrogen species contribute to the pathophysiology of inflammatory conditions. We have studied the effects of a novel superoxide scavenger, 4-dimethylamino-3′,4′-dimethoxychalcone (CH11) in macrophages and in vivo. CH11 has been shown to inhibit the chemiluminescence induced by zymosan in mouse peritoneal macrophages and the cytotoxic effects of superoxide. In the same cells, the modulation by superoxide of nitric oxide (NO) production in response to zymosan was investigated. CH11 was more effective than the membrane-permeable scavenger Tiron for inhibition of inducible nitric oxide synthase (iNOS) protein expression and nitrite production. We have shown that CH…

Anti-Inflammatory AgentsNitric Oxide Synthase Type IIPharmacologyCarrageenanNitric OxideBiochemistryGene Expression Regulation EnzymologicNitric oxideMicechemistry.chemical_compoundChalconeChalconesSuperoxidesIn vivoPhysiology (medical)AnimalsEdemaEnzyme InhibitorsRespiratory BurstInflammationTironbiologySuperoxideZymosanZymosanFree Radical ScavengersNitric oxide synthaseOxidative StresschemistryBiochemistryEicosanoidLuminescent Measurements12-Dihydroxybenzene-35-Disulfonic Acid Disodium SaltMacrophages Peritonealbiology.proteinFemaleTumor necrosis factor alphaNitric Oxide SynthaseFree Radical Biology and Medicine
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Peritoneal Cavity is a Route for Gut-Derived Microbial Signals to Promote Autoimmunity in Non-Obese Diabetic Mice

2015

Macrophages play a crucial role in innate immune reactions, and peritoneal macrophages (PMs) guard the sterility of this compartment mainly against microbial threat from the gut. Type 1 diabetes (T1D) is an autoimmune disease in which gut microbiota and gut immune system appear to contribute to disease pathogenesis. We have recently reported elevated free radical production and increased permeability of gut epithelium in non-obese diabetic (NOD) mice. Impaired barrier function could lead to bacterial leakage to the peritoneal cavity. To explore the consequences of impaired gut barrier function on extra-intestinal immune regulation, we characterized peritoneal lavage cells from young newly w…

Antigens Differentiation T-LymphocyteLipopolysaccharidesmedicine.medical_specialtymiceT-LymphocytesT cellBlotting WesternImmunologyWeaningNodBiologyta3111Peritoneal cavityImmune systemSpecies SpecificityAntigens CDMice Inbred NODInternal medicinediabeticmedicineAnimalsLectins C-TypeIntestinal Mucosamicrobial signalsCells CulturedNOD miceMice Inbred BALB CInnate immune systemTumor Necrosis Factor-alphanon-obeseMicrobiotaautoimmunityta1182ta3141General MedicineFlow CytometryGut EpitheliumIntestinesMice Inbred C57BLInterleukin-1 Receptor-Associated KinasesEndocrinologymedicine.anatomical_structureperitoneal cavityImmunologyMacrophages PeritonealTumor necrosis factor alphaInjections IntraperitonealSignal TransductionScandinavian Journal of Immunology
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Reduced VLDL clearance in ApoeNpc1 mice is associated with increased Pcsk9 and Idol expression and decreased hepatic LDL-receptor levels

2010

Niemann-Pick type C1 (NPC1) promotes the transport of LDL receptor (LDL-R)-derived cholesterol from late endosomes/lysosomes to other cellular compartments. NPC1-deficient cells showed impaired regulation of liver_X receptor (LXR) and sterol regulatory element-binding protein (SREBP) target genes. We observed that Apoe(-/-)Npc1(-/-) mice displayed a marked increase in total plasma cholesterol mainly due to increased VLDL, reflecting decreased clearance. Although nuclear SREBP-2 and Ldlr mRNA levels were increased in Apoe(-/-)Npc1(-/-) liver, LDL-R protein levels were decreased in association with marked induction of proprotein convertase subtilisin/kexin type 9 (Pcsk9) and inducible degrade…

Apolipoprotein EreceptorCholesterol VLDLLDL/metabolismMacrophages Peritoneal/cytologyBiochemistryMiceEndocrinologyhemic and lymphatic diseasesReceptorsOrphan Nuclear Receptors/geneticspolycyclic compoundsnuclear receptorCells CulturedResearch ArticlesLiver X ReceptorsMice KnockoutCulturedSterol Regulatory Element Binding Protein 2/geneticslipoproteinSerine EndopeptidasesIntracellular Signaling Peptides and ProteinsLamin Type AOrphan Nuclear ReceptorsTriglycerides/bloodCholesterolLiverProteins/geneticsKexinlipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9Sterol Regulatory Element Binding Protein 1Niemann-Pick diseaseSterol Regulatory Element Binding Protein 2medicine.medical_specialtyCellsKnockoutUbiquitin-Protein LigasesReceptors LDL/metabolismSerine Endopeptidases/geneticsQD415-436BiologyCholesterol/blooddigestive systemApolipoproteins ELiver/physiologySterol Regulatory Element Binding Protein 1/geneticsNiemann-Pick C1 ProteinInternal medicinemedicineAnimalsPeritoneal/cytologyCholesterol VLDL/metabolismUbiquitin-Protein Ligases/geneticsLiver X receptorTriglyceridesMacrophagesPCSK9Proteinsnutritional and metabolic diseasesVLDL/metabolismLamin Type A/metabolismCell BiologySterol regulatory element-binding proteinEndocrinologyReceptors LDLLDL receptorMacrophages PeritonealSterol regulatory element-binding protein 2atherosclerosisApolipoproteins E/geneticsLipoproteinJournal of Lipid Research
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Enhanced platelet thromboxane synthesis and reduced macrophage-dependent fibrinolytic activity related to oxidative stress in oral contraceptive-trea…

1996

Abstract In previous studies conducted in rats and in women, we have shown that oral contraceptive (OC) administration induced a platelet hyperaggregation simultaneously with an increased platelet lipid biosynthesis which might be related to lipid peroxidation. In the present study, we specifically studied the arachidonic acid and the fibrinolytic pathways in relation to the fatty acid composition in female rats treated for 6 weeks with OC (ethinyl estradiol plus lynestrenol). We found that platelets of treated animals were not only hyper-responsive to thrombin and ADP, but also to sodium arachidonate. In addition, the results of the thrombin-induced release of labeled arachidonic acid pre-…

Blood Plateletsmedicine.medical_specialtyErythrocytesPlatelet AggregationThromboxaneRadioimmunoassayLipid peroxidationRats Sprague-Dawleychemistry.chemical_compoundThromboxane A2Internal medicineLipid biosynthesisThromboembolismmedicineAnimalsArachidonic AcidFibrinolysisThromboxanesUrokinase-Type Plasminogen ActivatorRecombinant ProteinsRatsThromboxane B2Disease Models AnimalOxidative StressEndocrinology12-Hydroxyheptadecatrienoic acidchemistryMacrophages Peritoneal12-Hydroxyeicosatetraenoic acidArachidonic acidFemaleLipid PeroxidationCardiology and Cardiovascular MedicineContraceptives OralAtherosclerosis
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Heme oxygenase-1 induction and regulation in unstimulated mouse peritoneal macrophages

2003

Heme oxygenase-1 (HO-1) is a stress protein induced by a variety of stimuli in inflammatory cells. This study was set up to investigate the induction of this protein in unstimulated macrophages. Resident mouse peritoneal macrophages purified by adhesion and cultured in basal conditions strongly induced HO-1 in a time-dependent manner, with a peak at 20 hr. At the same time, low levels of nitrite accumulated in the culture medium and expression of nitric oxide synthase-2 (NOS-2) and NOS-3 protein was detected. Inhibition of NO production and/or NOS expression by incubating macrophages with different drugs inhibiting NOS activity or modulating the redox state of the cell, such as N-acetylcyst…

Blotting WesternInflammationNitric Oxidemedicine.disease_causeBiochemistryNitric oxideMicechemistry.chemical_compoundmedicineAnimalsMacrophageHemeCells CulturedPharmacologybiologyChemistryMembrane ProteinsEndogenous mediatorImmunohistochemistryCell biologyNitric oxide synthaseHeme oxygenaseBiochemistryEnzyme InductionHeme Oxygenase (Decyclizing)Macrophages Peritonealbiology.proteinNitric Oxide Synthasemedicine.symptomOxidation-ReductionHeme Oxygenase-1Oxidative stressBiochemical Pharmacology
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Impact of Glutathione Peroxidase-1 Deficiency on Macrophage Foam Cell Formation and Proliferation: Implications for Atherogenesis

2013

Clinical and experimental evidence suggests a protective role for the antioxidant enzyme glutathione peroxidase-1 (GPx-1) in the atherogenic process. GPx-1 deficiency accelerates atherosclerosis and increases lesion cellularity in ApoE(-/-) mice. However, the distribution of GPx-1 within the atherosclerotic lesion as well as the mechanisms leading to increased macrophage numbers in lesions is still unknown. Accordingly, the aims of the present study were (1) to analyze which cells express GPx-1 within atherosclerotic lesions and (2) to determine whether a lack of GPx-1 affects macrophage foam cell formation and cellular proliferation. Both in situ-hybridization and immunohistochemistry of l…

CD36 AntigensMAPK/ERK pathwayMouseMitogen-Activated Protein Kinase 3lcsh:MedicineGene ExpressionSignal transductionCardiovascularMiceMolecular cell biologyGlutathione Peroxidase GPX1lcsh:ScienceIn Situ HybridizationFoam cellMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryReverse Transcriptase Polymerase Chain ReactionKinaseSignaling cascadesScavenger Receptors Class AAnimal ModelsImmunohistochemistryLipoproteins LDLMedicineFemaleSignal transductionResearch ArticleMacrophage colony-stimulating factorMAPK signaling cascadesBlotting WesternBiologyCell GrowthModel OrganismsApolipoproteins EVascular BiologyAnimalsHumansProtein kinase ABiologyCell ProliferationGlutathione PeroxidaseMacrophage Colony-Stimulating Factorlcsh:RAtherosclerosisMolecular biologyMacrophages Peritoneallcsh:QMacrophage proliferationFoam CellsPLoS ONE
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Analysis of parathyroid graft rejection suggests alloantigen-specific production of nitric oxide by iNOS-positive intragraft macrophages

2009

Abstract Background During acute rejection of organ or tissue allografts T cells and macrophages are dominant infiltrating cells. CD4-positive T cells are important for the induction of allograft rejection and macrophages are important effector cells mediating cytotoxicity via production of nitric oxide (NO) by the inducible NO-synthase (iNOS). In the present study we analysed whether the destruction of primarily nonvascularised parathyroid allografts is also mediated by iNOS-positive macrophages. Methods Hypocalcaemic Lewis rats received parathyroid isografts (from Lewis donors) and allografts (from Wistar Furth donors), respectively, under the kidney capsule. Levels of serum calcium above…

CD4-Positive T-LymphocytesGraft RejectionMaleImmunologyThyroid GlandNitric Oxide Synthase Type IIRats Inbred WFInflammationCell CommunicationLymphocyte ActivationMajor histocompatibility complexNitric oxidechemistry.chemical_compoundAntigenCell MovementHistocompatibility AntigensmedicineAnimalsTransplantation HomologousImmunology and AllergyCytotoxic T cellMacrophageTransplantationbiologyChemistryMacrophage ActivationAntigens DifferentiationPeptide FragmentsRatsEnzyme ActivationTransplantationMononuclear cell infiltrationGene Expression RegulationRats Inbred LewImmunologyDisease ProgressionMacrophages Peritonealbiology.proteinCalciumImmunizationmedicine.symptomTransplant Immunology
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Impaired immune response to Candida albicans in aged mice

2006

The prevalence of opportunistic fungal infections has increased dramatically among the aged population in recent years. This work investigated the effect of ageing on murine defences against Candida albicans. Aged C57BL/6 mice that were experimentally infected intravenously had a significantly impaired survival and a higher tissue fungal burden compared with young mice. In vitro production of tumour necrosis factor (TNF)-α by macrophages from aged mice in response to yeast cells and hyphae of C. albicans was significantly lower than production by macrophages from young mice. In vitro production of cytokines, such as TNF-α and gamma interferon (IFN-γ), by antigen-stimulated splenocytes from …

CD4-Positive T-LymphocytesMicrobiology (medical)AgingNecrosisBlotting WesternHyphaeMicrobiologyMicrobiologyInterferon-gammaMiceImmune systemAntigenCandida albicansmedicineAnimalsCandida albicansAntibodies FungalCells CulturedbiologyTumor Necrosis Factor-alphaVaccinationCandidiasisGeneral Medicinebiology.organism_classificationAcquired immune systemCorpus albicansMice Inbred C57BLImmunoglobulin GInjections IntravenousImmunologyMacrophages Peritonealbiology.proteinFemaleTumor necrosis factor alphaDisease SusceptibilityFungal Vaccinesmedicine.symptomAntibodySpleenJournal of Medical Microbiology
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Differential expression of alternative H2-M isoforms in B cells, dendritic cells and macrophages by proinflammatory cytokines.

1999

Major histocompatibility (MHC) class II heterodimers bind peptides generated by degradation of endocytosed antigens and display them on the surface of antigen presenting cells (APCs) for recognition by CD4+ T cells. Efficient loading of MHC class II molecules with peptides is catalyzed by the MHC class II-like molecule H2-M. The coordinate regulation of MHC class II and H2-M expression is a prerequisite for efficient MHC class II/peptide assembly in APCs determining both the generation of the T cell repertoire in the thymus and cellular immune responses in the periphery. Here we show that expression of H2-M and MHC class II genes is coordinately and cell type-specific regulated in splenic B…

CD74ImmunologyAntigen presentationGenes MHC Class IICD1Antigen-Presenting CellsGene ExpressionIn Vitro TechniquesMHC Class II GeneMiceMHC class IAnimalsProtein IsoformsMolecular BiologyDNA PrimersMHC class IIB-LymphocytesHLA-D AntigensMice Inbred BALB CbiologyBase SequenceAntigen processingHistocompatibility Antigens Class IIDendritic CellsMHC restrictionMolecular biologybiology.proteinMacrophages PeritonealCytokinesInflammation MediatorsMolecular immunology
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Novel 1H‑Pyrrolo[2,3‑b]pyridine Derivative Nortopsentin Analogues: Synthesis and Antitumor Activity in Peritoneal Mesothelioma Experimental Models

2013

In this study, we describe the synthesis of new nortopsentin analogues, 1H-pyrrolo[2,3-b]pyridine derivatives and their biological effects in experimental models of diffuse malignant peritoneal mesothelioma (DMPM), a rare and rapidly fatal disease, poorly responsive to conventional therapies. The three most active compounds, 1f (3-[2-(5-fluoro-1-methyl-1H-indol-3- yl)-1,3-thiazol-4-yl]-1H-pyrrolo[2,3-b]pyridine), 3f (3-[2-(1H-indol-3-yl)-1,3- thiazol-4-yl]-1-methyl-1H-pyrrolo[2,3-b]pyridine), and 1l (3-[2-(5-fluoro-1- methyl-1H-indol-3-yl)-1,3-thiazol-4-yl]-1-methyl-1H-pyrrolo[2,3-b] pyridine), which were shown to act as cyclin-dependent kinase 1 inhibitors, consistently reduced DMPM cell p…

CDK1 inhibitorsmalignant peritoneal mesothelioma3‑b]pyridineNortopsentin Analogues1H‑Pyrrolo[21H‑Pyrrolo[23‑b]pyridineCDK1 inhibitorsNortopsentin AnalogueSettore CHIM/08 - Chimica Farmaceuticamalignant peritoneal mesothelioma; 1H‑Pyrrolo[2; 3‑b]pyridine; Nortopsentin Analogues; CDK1 inhibitors
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