Search results for "sulfones"

showing 6 items of 56 documents

Multigenerational study of the obesogen effects of bisphenol S after a perinatal exposure in C57BL6/J mice fed a high fat diet.

2021

International audience; Background : Bisphenol S is an endocrine disruptor exhibiting metabolic disturbances, especially following perinatal exposures. To date, no data are available on the obesogen effects of BPS in a mutligenerational issue.Objectives : We investigated obesogen effects of BPS in a multigenerational study by focusing on body weight, adipose tissue and plasma parameters in male and female mice.Methods : Pregnant C57BL6/J mice were exposed to BPS (1.5 μg/kg bw/day ie a human equivalent dose of 0.12 μg/kg bw/day) by drinking water from gestational day 0 to post natal day 21. All offsprings were fed with a high fat diet during 15 weeks. Body weight was monitored weekly and fat…

medicine.medical_specialty010504 meteorology & atmospheric sciences[SDV]Life Sciences [q-bio]Health Toxicology and MutagenesisAdipose tissue010501 environmental sciencesToxicologyDiet High-Fat01 natural scienceschemistry.chemical_compoundMiceNEFAPhenolsPregnancyLow dose exposureInternal medicinemedicineLipolysisAnimalsObesogenSulfonesPeri-natal exposure0105 earth and related environmental sciences2. Zero hungerTriglyceridebusiness.industryGeneral Medicinemedicine.diseasePollutionEndocrinologyTransgenerational effectschemistryEndocrine disruptorPrenatal Exposure Delayed EffectsLipogenesisFemalebusinessDyslipidemiaObesogenEnvironmental pollution (Barking, Essex : 1987)
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Acetylcholine mediates the release of IL-8 in human bronchial epithelial cells by a NFkB/ERK-dependent mechanism

2007

Acetylcholine may play a role in cell activation and airway inflammation. We evaluated the levels of both mRNA and protein of muscarinic M(1), M(2), M(3) receptors in human bronchial epithelial cell line (16HBE). 16HBE cells were also stimulated with acetylcholine and extracellular signal-regulated kinase1/2 (ERK1/2) and NFkB pathway activation as well as the IL-8 release was assessed in the presence or absence of the inhibitor of Protein-kinase (PKC) (GF109203X), of the inhibitor of mitogenic activated protein-kinase kinase (MAPKK) (PDO9805), of the inhibitor of kinaseB-alpha phosphorilation (pIkBalpha) (BAY11-7082), and of muscarinic receptor antagonists tiotropium bromide, 4-Diphenylacet…

medicine.medical_specialtyIndolesNeutrophilsScopolamine DerivativesBronchiMuscarinic AntagonistsBiologyPharmacologyMaleimideschemistry.chemical_compoundPiperidinesInternal medicineNitrilesMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptormedicineHumansRNA MessengerSulfonesTiotropium BromideProtein Kinase CCell Line TransformedAcetylcholine receptorFlavonoidsMitogen-Activated Protein Kinase 1PharmacologyMitogen-Activated Protein Kinase 3Gallamine TriethiodideInterleukin-8NF-kappa BMuscarinic acetylcholine receptor M3Epithelial CellsMuscarinic acetylcholine receptor M2PirenzepineMuscarinic acetylcholine receptor M1Receptors MuscarinicAcetylcholineChemotaxis LeukocyteEndocrinologychemistryTelenzepineAcetylcholinemedicine.drugEuropean Journal of Pharmacology
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TREATMENT WITH SILDENAFIL PREVENTS IMPAIRMENT OF LEARNING IN RATS BORN TO PRE-ECLAMPTIC MOTHERS

2010

Pre-eclampsia is an important hypertensive pregnancy disorder and a main cause of maternal and fetal morbidity and mortality Children born from mothers with preeclampsia may present cognitive deficits The mechanisms leading to this cognitive impairment remain unclear and no treatments to improve it have been tested Pre-eclampsia is associated with impaired regulation of the nitric oxide 3 5 guanosine monophosphate cyclic (cGMP) pathway, which modulates some cognitive functions We hypothesized that alterations in the NO-cGMP pathway would be involved in the mechanisms leading to cognitive impairment in rats born to pre-eclamptic mothers and that treatment with sildenafil an inhibitor of the …

medicine.medical_specialtyMicrodialysisSildenafilPhosphodiesterase InhibitorsMicrodialysisGlutamic AcidBlood PressureMotor ActivityNitric OxidePiperazinesSildenafil CitrateNitric oxideDiscrimination Learningchemistry.chemical_compoundPre-EclampsiaIn vivoPregnancynitric oxideInternal medicineCerebellummedicineAnimalsLearningSulfonesMaze LearningCyclic GMPFetusbiologyGeneral NeurosciencePhosphodiesteraseCognitionpre eclampsiaRatsNitric oxide synthaseEndocrinologyNG-Nitroarginine Methyl EsterchemistryPurinesPrenatal Exposure Delayed Effectsbiology.proteinFemale3-5 guanosine monophosphate cyclic (cGMP)Nitric Oxide SynthasePsychologycognitive function sildenafil
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cGMP MODULATES STEM CELLS DIFFERENTIATION TO NEURONS IN BRAIN IN VIVO

2010

During brain development neural stem cells may differentiate to neurons or to other cell types. The aim of this work was to assess the role of cGMP (cyclic GMP) in the modulation of differentiation of neural stem cells to neurons or non-neuronal cells. cGMP in brain of fetuses was reduced to 46% of controls by treating pregnant rats with nitroarginine-methylester (L-NAME) and was restored by co-treatment with sildenafil.Reducing cGMP during brain development leads to reduced differentiation of stem cells to neurons and increased differentiation to non-neuronal cells. The number of neurons in the prefrontal cortex originated from stem cells proliferating on gestational day 14 was 715 +/- 14/…

medicine.medical_specialtyPhosphodiesterase InhibitorsNeurogenesissildenafilHippocampusPrefrontal CortexApoptosisHippocampusPiperazinesSildenafil Citratenitric oxideNeurosphereInternal medicinemedicineAnimalsratSulfonesEnzyme InhibitorsRats WistarCyclic GMPNitritesCerebral CortexNeuronsNitratesbiologyGeneral NeuroscienceStem CellsBrainCell DifferentiationNeural stem cellRatsNeuroepithelial cellmedicine.anatomical_structureEndocrinologyNG-Nitroarginine Methyl Esternervous systemPurinesbiology.proteinNeuronStem cellNeuNAdult stem cell
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Sodium-hydrogen exchange inhibition: novel strategy to prevent myocardial injury following ischemia and reperfusion.

1999

Activation of Na+/H+ exchange and subsequent calcium overload in cardiac myocytes appear to play an important role in myocardial tissue injury following ischemia and reperfusion. Results of several in vitro studies in isolated myocytes and heart preparations and in vivo studies in pigs and rats have suggested that inhibition of Na+/H+ exchange is an effective means to prevent lethal reperfusion injury, arrhythmia, and improve myocardial contractile dysfunction. In patients with acute myocardial infarction (MI), any preventive agent is administered immediately before or shortly after reperfusion, rather than before the occurrence of coronary occlusion. The direct interventional approach to t…

medicine.medical_specialtySodium-Hydrogen Exchangersmedicine.medical_treatmentPremedicationIschemiaMyocardial InfarctionMyocardial Reperfusion InjuryPilot ProjectsGuanidineschemistry.chemical_compoundInternal medicineAngioplastyLactate dehydrogenasemedicineAnimalsHumansMyocardial infarctionSulfonesAngioplasty Balloon CoronaryInfusions IntravenousCariporidebiologybusiness.industrymedicine.diseaseRatschemistryCoronary occlusionAnesthesiaCardiologybiology.proteinCreatine kinaseCardiology and Cardiovascular MedicinebusinessReperfusion injuryAnti-Arrhythmia AgentsThe American journal of cardiology
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Cigarette smoke-induced pulmonary endothelial dysfunction is partially suppressed by sildenafil.

2009

Abstract Cigarette smoke mediated oxidative stress and endothelial dysfunction are important processes in the pathogenesis of several lung disorders. In this study we evaluated the effect of PDE5 inhibition on pulmonary artery endothelial dysfunction induced by cigarette smoke in vitro . Human pulmonary artery endothelial cells (HPAEC) were incubated in the absence or presence of PDE5 inhibitor sildenafil (10 nM–1 μM), PKG agonist 8-Br-cGMP (1 mM), or the antioxidants dyphenyleneiodonium (DPI 1 μM) and N -acetylcysteine (NAC 1 mM) for 30 min. Then, cigarette smoke extract (CSE) was added for 24 h. CSE (2.5–10%)-induced ROS generation was suppressed by DPI, and partially reversed by sildenaf…

medicine.medical_specialtymedicine.drug_mechanism_of_actionSildenafilVasodilator AgentsPharmaceutical ScienceEnzyme-Linked Immunosorbent Assaymedicine.disease_causeNitric OxidePolymerase Chain ReactionPiperazinesSildenafil CitrateAcetylcysteinechemistry.chemical_compoundInternal medicineSmokeparasitic diseasesTobaccomedicineHumansSulfonesEndothelial dysfunctionPhosphodiesterase inhibitorLungCells CulturedDNA PrimersbiologyBase Sequencebusiness.industrymedicine.diseaseEndothelial stem cellEndocrinologychemistryEnzyme inhibitorPurinescardiovascular systembiology.proteinEndothelium VascularbusinessPhosphodiesterase 5 inhibitorOxidative stressmedicine.drugEuropean journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
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