Search results for "Prostaglandin E"

showing 8 items of 98 documents

Platelet Activity and Blood Lipid Changes in Diabetes Mellitus

1984

An altered platelet function can often be found in diabetes mellitus (2, 3, 4, 10, 13, 16, 17, 23, 24). Several studies have pointed towards an increased sensitivity of platelets to ADP induced aggregation (3, 6, 23) in diabetic patients; this phenomenon can also be found in diabetics without apparent vasculopathy and in subjects with altered glucose tolerance (3, 23).

medicine.medical_specialtybusiness.industryfood and beveragesBlood lipidsDiabetic retinopathyDiabetic angiopathymedicine.diseaseMalondialdehydechemistry.chemical_compoundEndocrinologychemistryInternal medicineDiabetes mellitusmedicinePlateletPlatelet activationbusinessProstaglandin endoperoxide
researchProduct

Interleukin-6 production in "normal" and HTLV-1 tax-expressing brain-specific endothelial cells.

1993

Abnormal cytokine production can contribute in many instances to the development of pathology. Our study focuses on the regulation of interleukin (IL)-6 production in vitro in brain-specific endothelial cells (BEC) under physiological conditions and in a model of human T leukemia virus-1 (HTLV-1) infection. IL-6 production was strongly up-regulated in a dose-dependent mode upon exposure to recombinant IL-1 beta, although nearly not detectable in unstimulated BEC. This induction of IL-6 production could be achieved by reagents known to increase intracellular levels of cAMP, such as forskolin, prostaglandin E or pentoxifylline. Furthermore, transcription and production of IL-6 was inducible b…

medicine.medical_specialtymedicine.medical_treatmentImmunologyTransfectionchemistry.chemical_compoundMiceInternal medicinemedicineImmunology and AllergyAnimalsRNA MessengerInterleukin 6health care economics and organizationsCells CulturedMice Inbred BALB CForskolinbiologyInterleukin-6Genes pXInterleukinBrainTransfectionHTLV-I InfectionsCell biologyEndothelial stem cellCytokineEndocrinologychemistryBucladesineSecond messenger systembiology.proteinEndothelium VascularProstaglandin EEuropean journal of immunology
researchProduct

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
researchProduct

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
researchProduct

Anti-senescence and Anti-inflammatory Effects of the C-terminal Moiety of PTHrP Peptides in OA Osteoblasts.

2016

Osteoarthritis (OA) is characterized by degenerative changes in the whole joint leading to physical disability in the elderly population. This condition is associated with altered bone metabolism in subchondral areas suggesting that therapeutic strategies aimed at modifying bone cell metabolism may be of interest. We have investigated the effects of several parathyroid hormone-related protein (PTHrP)-derived peptides (1-37): (N-terminal), (107-111) and (107-139) (C-terminal) on senescence features induced by inflammatory stress in human OA osteoblasts. Incubation of these primary cells with interleukin(IL)-1β led to an increased expression of senescence markers senescence-associated-β-galac…

musculoskeletal diseases0301 basic medicineSenescenceMaleAgingmedicine.medical_specialtyInterleukin-1betaParathyroid hormoneFluorescent Antibody TechniqueReal-Time Polymerase Chain ReactionDinoprostone03 medical and health sciencesDownregulation and upregulationInternal medicineBone cellOsteoarthritismedicineHumansProstaglandin E2Cells CulturedCellular SenescenceAgedOsteoblastsParathyroid hormone-related proteinbusiness.industryInterleukin-6Tumor Necrosis Factor-alphaParathyroid Hormone-Related ProteinPeptide Fragments030104 developmental biologyEndocrinologyTumor necrosis factor alphaFemaleGeriatrics and GerontologyInflammation MediatorsbusinessCell aginghormones hormone substitutes and hormone antagonistsmedicine.drugThe journals of gerontology. Series A, Biological sciences and medical sciences
researchProduct

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
researchProduct

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
researchProduct

Inhibition of Rho modulates cytokine-induced prostaglandin E2 formation in renal mesangial cells.

2003

Stimulation of rat mesangial cells for 24 h with interleukin-1β(IL-1β) plus forskolin (Fk) leads to a marked increase in prostaglandin E 2 (PGE 2 ) synthesis. This effect is further enhanced by the small G-protein Rho inhibitor toxin A. A similar increase in PGE 2 formation is obtained with Y27632, a Rho-dependent kinase inhibitor, and with lovastatin, a hydroxymethylglutaryl-coenzyme A inhibitor which depletes cells from geranylgeranyl moieties and thus blocks Rho activation. In parallel to the increased PGE 2 synthesis, a potentiation of IL-1β-induced secretory group IIA phospholipases A 2 (sPLA 2 -IIA) protein expression also occurs by Rho inhibition. However, only toxin A triggers an in…

rho GTP-Binding Proteinsmedicine.medical_treatmentBlotting WesternProstaglandinBiologyDinoprostonePhospholipases Achemistry.chemical_compoundmedicineAnimalsProstaglandin E2Molecular BiologyCells CulturedForskolinMesangial cellKinaseColforsinCell BiologyMolecular biologyGlomerular MesangiumRatsPhospholipases A2Cytokinechemistrylipids (amino acids peptides and proteins)Lovastatinmedicine.drugProstaglandin EInterleukin-1Biochimica et biophysica acta
researchProduct