Search results for "Cyclooxygenase 2"

showing 7 items of 137 documents

Progestogens stimulate prostacyclin production by human endothelial cells.

2005

BACKGROUND: The effects of progestogens on endothelial physiology are poorly studied. Prostacyclin is a potent vasodilator synthesized by two isoforms of cyclooxygenase (COX) in endothelium. We examined the effects of two clinically used progestogens, progesterone and medroxyprogesterone acetate (MPA), on prostacyclin production by cultured human umbilical vein endothelial cells (HUVEC) and the possible role of progesterone receptors and both COX enzymes. METHODS: Cells were exposed to 1-100 nmol/l of either progesterone or MPA and prostacyclin production was measured in culture medium. RESULTS: Both progestogens significantly increased prostacyclin release in a time- and dose-dependent man…

medicine.medical_specialtyUmbilical VeinsEndotheliumProstacyclinMedroxyprogesterone AcetateUmbilical veinInternal medicineProgesterone receptormedicineMedroxyprogesterone acetateHumansCyclooxygenase InhibitorsReceptorCells CulturedNitrobenzenesProgesteroneSulfonamidesbiologyCyclooxygenase 2 InhibitorsDose-Response Relationship DrugEstradiolRehabilitationObstetrics and GynecologyEndothelial CellsMembrane ProteinsEpoprostenolEndothelial stem cellMifepristoneEndocrinologymedicine.anatomical_structureReproductive MedicineCyclooxygenase 2Prostaglandin-Endoperoxide Synthasescardiovascular systembiology.proteinCyclooxygenase 1PyrazolesCyclooxygenaseEndothelium VascularProgestinsReceptors Progesteronemedicine.drugHuman reproduction (Oxford, England)
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Inhibition of the NF-κB Signaling Pathway Mediates the Anti-inflammatory Effects of Petrosaspongiolide M

2003

Petrosaspongiolide M (PT) is a potent secretory phospholipase A(2) inhibitor and anti-inflammatory agent. This marine metabolite reduced the production of nitrite, prostaglandin E(2), and tumor necrosis factor-alpha in the mouse air pouch injected with zymosan. These effects were also observed in mouse peritoneal macrophages stimulated with zymosan. Inhibition of these inflammatory mediators was related to reductions in inducible nitric oxide synthase, cyclo-oxygenase-2, and tumor necrosis factor-alpha expression. Since nuclear factor-kappaB (NF-kappaB) appears to play a central role in the transcriptional regulation of these proteins by macrophages, we investigated the effects of PT on thi…

medicine.medical_treatmentAnti-Inflammatory AgentsNitric Oxide Synthase Type IIBiochemistryDinoprostoneMicechemistry.chemical_compoundPhospholipase A2NF-KappaB Inhibitor alphaCell MovementmedicineAnimalsRNA MessengerOleanolic AcidPhosphorylationNitritesPharmacologybiologyTumor Necrosis Factor-alphaZymosanNF-kappa BZymosanBiological TransportNF-κBDNACell biologyIsoenzymesNitric oxide synthaseIκBαCytokinechemistryBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesModels AnimalMacrophages Peritonealbiology.proteinCytokinesI-kappa B ProteinsTumor necrosis factor alphaNitric Oxide SynthaseSignal TransductionProstaglandin E
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A pyrroloquinazoline derivative with anti-inflammatory and analgesic activity by dual inhibition of cyclo-oxygenase-2 and 5-lipoxygenase

2002

Abstract In a previous study, we reported a new pyrroloquinazoline derivative, 3-(4′-acetoxy-3′,5′-dimethoxy)benzylidene-1,2-dihydropyrrolo[2,1- b ]quinazoline-9-one (PQ), which inhibited human purified 5-lipoxygenase activity and prostaglandin E 2 release in lipopolysaccharide-stimulated RAW 264.7 cells. In the present work, we show that PQ inhibits cyclo-oxygenase-2 activity in intact cell assays (human monocytes) and purified enzyme preparations (ovine isoenzymes) without affecting cyclo-oxygenase-1 activity. This behaviour was confirmed in vivo by using the zymosan-injected mouse air pouch model, where PQ caused a marked reduction in cell migration and leukotriene B 4 levels at 4 h, as …

medicine.medical_treatmentPharmacologyMonocytesMicechemistry.chemical_compoundIn vivomedicineAnimalsEdemaHumansCyclooxygenase InhibitorsPyrrolesLipoxygenase InhibitorsEnzyme InhibitorsProstaglandin E2Pain MeasurementPharmacologyAnalgesicsArachidonate 5-LipoxygenaseSheepCyclooxygenase 2 InhibitorsDose-Response Relationship DrugbiologyChemistryAnti-Inflammatory Agents Non-SteroidalZymosanMembrane ProteinsBiological activityIsoenzymesBiochemistryMechanism of actionCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesEnzyme inhibitorArachidonate 5-lipoxygenaseQuinazolinesQuinolinesbiology.proteinFemalemedicine.symptomProstaglandin Emedicine.drug
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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COX-2 expression in chondrosarcoma: A role for celecoxib treatment?

2010

Chondrosarcomas are resistant to conventional chemo- and radiotherapy. A subset of chondrosarcomas arises secondarily in the benign tumour syndromes enchondromatosis (EC) and multiple osteochondromas (MO), and prevention of tumour development would greatly improve prognosis. We therefore investigated the effect of selective COX-2 inhibition on chondrosarcoma growth. COX-2 expression was studied in central- and peripheral cartilaginous tumours. The effect of COX-2 inhibition was assessed in four high-grade chondrosarcoma cell lines using celecoxib and NS-398 treatment. COX-2 activity (prostaglandin E-2 (PGE(2)) ELISA) and cell viability were measured. The (prophylactic) effect of celecoxib o…

musculoskeletal diseasesMaleCancer ResearchPathologymedicine.medical_specialtyCell Survivalmedicine.medical_treatmentChondrosarcomaDrug Evaluation PreclinicalMice NudeAntineoplastic AgentsBone NeoplasmsMiceIn vivomedicineTumor Cells CulturedAnimalsHumansViability assaySulfonamidesCyclooxygenase 2 Inhibitorsbusiness.industryCartilagemedicine.diseaseXenograft Model Antitumor AssaysRadiation therapyDisease Models Animalmedicine.anatomical_structureOncologyBone tumours Chondrosarcoma COX-2 inhibition Therapy Xenograft familial adenomatous polyposis cell-line cyclooxygenase-2 inhibitor trial tumors establishment emphasis origin boneCell cultureCelecoxibCyclooxygenase 2CelecoxibPyrazolesChondrosarcomabusinessmedicine.drugProstaglandin E
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Sicilian pistachio (Pistacia vera L.) nut inhibits expression and release of inflammatory mediators and reverts the increase of paracellular permeabi…

2014

Background Dietary approaches to control inflammatory bowel diseases (IBD) may include proanthocyanidin-rich foods. Our previous research showed that a hydrophilic extract from Sicilian pistachio nut (HPE) contains sub- stantial amounts of proanthocyanidins and possesses anti- inflammatory activities. Purpose We studied the effects of HPE and of its poly- meric proanthocyanidin fraction (PPF) in a cell model that simulated some conditions of IBD, consisting of interleukin (IL)-1b-stimulated Caco-2 cells. Methods HPE was prepared by Pistacia vera L. nuts, and PPF was isolated from HPE by adsorbance chromatogra- phy. Proanthocyanidins were quantified as anthocyanidins after acidic hydrolysis.…

musculoskeletal diseasesPistachio nut Inflammation Intestinal epithelium Polyphenols Proanthocyanidinscongenital hereditary and neonatal diseases and abnormalitiesCellInterleukin-1betaAnti-Inflammatory AgentsMedicine (miscellaneous)BiologyPharmacologyPermeabilityCell membraneSettore BIO/10 - BiochimicamedicineHumansNutsProanthocyanidinsViability assayIntestinal MucosaCell ProliferationNutrition and DieteticsPistaciaInterleukin-6Interleukin-8NF-kappa BEpithelial Cellsbiology.organism_classificationIntestinal epitheliumIntestinesmedicine.anatomical_structureProanthocyanidinBiochemistryCaco-2Cyclooxygenase 2Paracellular transportPistaciaCaco-2 Cells
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Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

2008

Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…

musculoskeletal diseasesmedicine.medical_treatmentImmunologyAnti-Inflammatory AgentsDrug Evaluation PreclinicalType II collagenArthritisInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]DinoprostoneGeneral Biochemistry Genetics and Molecular BiologyMiceRheumatologyOrganometallic CompoundsPerception and Action [DCN 1]medicineAnimalsImmunology and AllergyChronic inflammation and autoimmunity [UMCN 4.2]Dose-Response Relationship Drugbiologybusiness.industryRANK LigandInterleukinIntercellular Adhesion Molecule-1medicine.diseaseArthritis ExperimentalPathogenesis and modulation of inflammation [N4i 1]Cellular infiltrationCyclooxygenase 2Mice Inbred DBARANKLImmunologybiology.proteinCytokinesTumor necrosis factor alphaMicrobial pathogenesis and host defense [UMCN 4.1]Inflammation Mediatorsmedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1Immunity infection and tissue repair [NCMLS 1]Prostaglandin E
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