Search results for "PROSTAGLANDIN"

showing 10 items of 232 documents

Age-related changes in linoleic acid bioconversion by isolated hepatocytes from spontaneously hypertensive and normotensive rats

1994

This study points out the hepatocyte interconversion of the linoleic acid family during hypertension. Hepatocyte delta 6 desaturase activity was higher in 1 month-old spontaneously hypertensive rats than in normotensive controls. A similar tendency was observed in 6 month-old SHR. delta 5 desaturase activity was higher only in 1 month-old spontaneously hypertensive rats as compared to controls. Desaturase activities were particularly high at the age of 6 months. The hepatocyte fatty acid composition showed an impairment of n-6 polyunsaturated fatty acid metabolism in spontaneously hypertensive animals. Changes were greater in the young prehypertensive rats than in adults. A storage of n-3 l…

Agingmedicine.medical_specialtyClinical chemistryLinoleic acidClinical BiochemistryProstaglandinRats Inbred WKYLinoleic Acidchemistry.chemical_compoundRats Inbred SHRInternal medicinemedicineAnimalsMolecular Biologychemistry.chemical_classificationKidneyFatty AcidsCell BiologyGeneral MedicineMetabolismPeroxisomeRatsEndocrinologymedicine.anatomical_structureLinoleic AcidsLiverchemistryHepatocyteHypertensionPolyunsaturated fatty acidMolecular and Cellular Biochemistry
researchProduct

Prostacyclin receptor desensitization is a reversible phenomenon in human platelets.

1997

Background Long-term exposure of platelets to endogenous or exogenous prostacyclin or its analogues might result in desensitization of the platelet prostacyclin receptor in vitro and in vivo accompanied by a loss in receptor density on the platelet surface and a reduced sensitivity toward the inhibitory effects of prostacyclins. However, the reversibility of this process in platelets has not yet been investigated. Methods and Results Human platelets desensitized by the chemically stable prostacyclin analogue iloprost showed a significant reduction in [ 3 H]-iloprost binding sites that was reversed by saponin permeabilization. This indicates functionally active internalized prostacyclin rec…

AgonistBlood PlateletsMalemedicine.medical_specialtyCell Membrane Permeabilitymedicine.drug_classReceptors ProstaglandinProstaglandinProstacyclinReceptors EpoprostenolProstacyclin receptor bindingchemistry.chemical_compoundReference ValuesPhysiology (medical)Internal medicinemedicineCyclic AMPHumansPlateletIloprostProstacyclin receptorbusiness.industryEndocrinologychemistrycardiovascular systemPlatelet aggregation inhibitorlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicinebusinessPlatelet Aggregation Inhibitorsmedicine.drugIloprostCirculation
researchProduct

Endothelin Antagonism: Effects of FP Receptor Agonists Prostaglandin F2αand Fluprostenol on Trabecular Meshwork Contractility

2006

Purpose This study analyzes additional mechanisms behind the ocular hypotensive effect of prostaglandin F (PGF) receptor (FP receptor) agonists PGF2alpha and fluprostenol (fluprostenol-isopropyl ester [travoprost]), which reduce intraocular pressure (IOP) in patients with glaucoma probably by enhancing uveoscleral flow. The trabecular meshwork (TM) is actively involved in IOP regulation through contractile mechanisms. Contractility of TM is induced by endothelin (ET)-1, a possible pathogenic factor in glaucoma. The involvement of FP receptor agonists in the ET-1 effects on TM function was studied. Methods The effects of FP receptor agonists on contractility of bovine TM (BTM) were investiga…

Agonistmedicine.medical_specialtyCarbacholmedicine.drug_classBlotting WesternReceptors ProstaglandinDinoprostContractilityTravoprostTrabecular MeshworkInternal medicinemedicineAnimalsReceptorCells CulturedEndothelin-1ChemistryCloprostenolMuscle SmoothEndothelin 1medicine.anatomical_structureProstaglandin F2alphaEndocrinologyCalciumCattleTrabecular meshworkFura-2Endothelin receptorMuscle Contractionmedicine.drugInvestigative Opthalmology & Visual Science
researchProduct

Prostaglandin D2 regulates joint inflammation and destruction in murine collagen-induced arthritis.

2012

Item does not contain fulltext OBJECTIVE: Prostaglandin D2 (PGD2) may exert proinflammatory or antiinflammatory effects in different biologic systems. Although this prostanoid and the enzymes responsible for its synthesis are up-regulated by interleukin-1beta (IL-1beta) in human chondrocytes in vitro, the role of PGD2 in arthritis remains unclear. This study was undertaken to investigate the role of PGD2 in the inflammatory response and in joint destruction during the development of collagen-induced arthritis (CIA) in mice. METHODS: PGD2 and cytokine levels in mice with CIA were determined by enzyme-linked immunosorbent assay. Expression of hematopoietic PGD synthase (h-PGDS), lipocalin-typ…

Agonistmusculoskeletal diseasesmedicine.medical_specialtyIndolesmedicine.drug_classmedicine.medical_treatmentChemokine CXCL1ImmunologyInterleukin-1betaReceptors ProstaglandinArthritisInflammationProinflammatory cytokinechemistry.chemical_compoundMiceRheumatologyBone MarrowInternal medicinemedicineImmunology and AllergyAnimalsPharmacology (medical)Receptors ImmunologicReceptorintegumentary systembusiness.industryProstaglandin D2Hydantoinsmedicine.diseaseArthritis ExperimentalLipocalinsHindlimbInterleukin-10Up-RegulationIntramolecular OxidoreductasesInterleukin 10CytokineEndocrinologychemistryMice Inbred DBACytokinesJointslipids (amino acids peptides and proteins)Prostaglandin D2Immune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]medicine.symptombusiness
researchProduct

Mast cells in allergic asthma and beyond.

2010

Mast cells have been regarded for a long time as effector cells in IgE mediated type I reactions and in host defence against parasites. However, they are resident in all environmental exposed tissues and express a wide variety of receptors, suggesting that these cells can also function as sentinels in innate immune responses. Indeed, studies have demonstrated an important role of mast cells during the induction of life-saving antibacterial responses. Furthermore, recent findings have shown that mast cells promote and modulate the development of adaptive immune responses, making them an important hinge of innate and acquired immunity. In addition, mast cells and several mast cell-produced me…

AllergyLeukotrienesmast cellsReview ArticleImmunoglobulin EModels BiologicalClassical complement pathwaychemistry.chemical_compoundMiceImmune systemAnti-Infective AgentsThymic Stromal LymphopoietinmedicineHypersensitivityAnimalsHumansmediatorsInnate immune systembiologyTumor Necrosis Factor-alphaGeneral MedicineImmunoglobulin Emedicine.diseaseAcquired immune systemallergyAsthmachemistryImmune SystemImmunologybiology.proteinProstaglandinsCytokinesTumor necrosis factor alphaHistamineHistamineYonsei medical journal
researchProduct

Novel Insights and Therapeutical Applications in the Field of Inhibitors of COX-2

2004

The discovery of the two isoenzymes COX-1 and COX-2 and the knowledge of their function, localisation and regulation has initiated the development of COX-2 selective inhibitors (coxibs). Inducible COX-2 at the peripheral site of inflammation has been detected in the early 1990s, the involvement of recently detected spinal COX-2 has led to new insights into mechanisms of pain and may explain analgesic and antipyretic properties of COX-2 selective inhibitors. The coxibs rofecoxib and celecoxib have been introduced into therapy and seem to offer some advantages over the classical non-selective NSAIDs. The search for new COX-2 inhibitors is going on, the development of etoricoxib and lumiracox…

AnalgesicArthritisPharmacologyBioinformaticsBiochemistryProstate cancerDrug DiscoverymedicineAnimalsHumansCyclooxygenase InhibitorsRofecoxibPharmacologyCyclooxygenase 2 Inhibitorsbusiness.industryOrganic ChemistryMembrane Proteinsmedicine.diseaseTolerabilityCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesCelecoxibMolecular MedicineLumiracoxibbusinessEtoricoxibmedicine.drugCurrent Medicinal Chemistry
researchProduct

Synthesis of complement by macrophages and modulation of their functions through complement activation.

1983

During the last decade considerable progress has been made to characterize intimate functional links between macrophages, a major cellular component of immunoinflammatory responses, and the complement system representing the major humoral mediator of inflammation. Macrophages of various species and tissue sites have been shown to synthesize and release most of the complement components providing these cells with their own \ldpericellular\rd complement system. Circumstantial evidence for the assembly of both classical and alternative pathway convertases has been adduced. An intricate network of feedback loops involving endogenous and extrinsic factors operates to adjust complement production…

AnaphylatoxinsImmunologyComplement Pathway AlternativeGuinea PigsComplement receptorBiologyIn Vitro TechniquesMonocytesClassical complement pathwayMiceImmune systemPhagocytosisComplement C1AnimalsHumansAnaphylatoxinComplement ActivationComplement component 3MacrophagesComplement C5Complement C4General MedicineComplement C3Complement System ProteinsComplement C2Complement systemCell biologyReceptors ComplementImmunologyAlternative complement pathwayComplement C3aProstaglandinsComplement component 5aSpringer seminars in immunopathology
researchProduct

Effects of cimetidine, atropine and prostaglandin E2 on rat mucosal erosions produced by intragastric distension

1980

Abstract The effects of three typical antisecretory agents: cimetidine, atrophine and prostaglandin E2 were compared on an acute rat gastric ulcer model which consisted of perfusing the stomach continuously, at a high intraluminal pressure (120 mm H2O), with a simulated gastric juice (0.1 M HCl plus 600 mg pepsin/1). As the acid and pepsin are given exogenously the inhibitory action of the antisecretory drugs is obviated in this model. Cimetidine and atropine failed to reduce gastric erosions, whereas prostaglandin E2 markedly reduced the severity of the mucosal lesions with respect to control values. Long-term treatment with cimetidine also failed to increase the resistance of the gastric …

AtropineMalemedicine.medical_treatmentPharmacologyGuanidinesPepsinmedicineGastric mucosaAnimalsStomach UlcerProstaglandin E2CimetidinePharmacologyGastric Juicebiologybusiness.industryProstaglandins EGastric distensionStomachdigestive oral and skin physiologyRatsDisease Models AnimalAtropinemedicine.anatomical_structureAnesthesiabiology.proteinmedicine.symptomCimetidinebusinessProstaglandin Emedicine.drugEuropean Journal of Pharmacology
researchProduct

Heme oxygenase-1 induction by nitric oxide in RAW 264.7 macrophages is upregulated by a cyclo-oxygenase-2 inhibitor.

2001

Unstimulated RAW 264.7 macrophages express negligible heme oxygenase-1 (HO-1) protein but incubation with the nitric oxide (NO) donor spermine nonoate (SPNO) induced HO-1 and weakly cyclo-oxygenase-2 (COX-2) protein. This effect was potentiated by coincubation with the COX-2 selective inhibitor, SC58125. Cells incubated with SPNO showed a strong increase in HO-1 mRNA levels after 4 h with a significant potentiation in the presence of SC58125, which did not modify HO-1 mRNA stability. The induction of HO-1 by NO and its potentiation by anti-inflammatory agents may play a role in inflammatory and immune responses.

BiophysicsSpermineNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundMiceDownregulation and upregulationMacrophageAnimalsCyclooxygenase InhibitorsRNA MessengerMolecular BiologyHemeCyclooxygenase 2 InhibitorsMacrophagesMembrane ProteinsLong-term potentiationDrug SynergismMolecular biologyUp-RegulationHeme oxygenaseIsoenzymeschemistryBiochemistryCell cultureCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesHeme Oxygenase (Decyclizing)PyrazolesNitrogen OxidesSpermineHeme Oxygenase-1Biochimica et biophysica acta
researchProduct

Mechanisms involved in the relaxant action of testosterone in the renal artery from male normoglycemic and diabetic rabbits.

2009

Kidney disease is a frequent complication in diabetes, and significant differences have been reported between male and female patients. Our working hypothesis was that diabetes might modify the vascular actions of testosterone in isolated rabbit renal arteries and the mechanisms involved in these actions. Testosterone (10(-8) to 10(-4)M) induced relaxation of precontracted arteries, without significant differences between control and diabetic rabbits. Both in control and diabetic rabbits endothelium removal inhibited testosterone relaxant action. In arteries with endothelium, incubation with indomethacin (10(-5)M), N(G)-nitro-l-arginine (10(-5)M) or tetraethylammonium (10(-5)M) did not modi…

Blood GlucoseMalemedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIProstacyclinVasodilationNitroarginineMuscle Smooth VascularDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Renal ArteryEnosInternal medicinemedicine.arteryDiabetes mellitusmedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsProstaglandins ITestosteroneRenal arteryPharmacologybiologyDose-Response Relationship Drugbusiness.industryTetraethylammoniumTestosterone (patch)medicine.diseasebiology.organism_classificationVasodilationEndocrinologymedicine.anatomical_structureCyclooxygenase 2Cyclooxygenase 1PotassiumCalciumEndothelium VascularRabbitsbusinessmedicine.drugSignal TransductionPharmacological research
researchProduct