Search results for "mice"

showing 10 items of 6027 documents

Mas receptor is involved in the estrogen-receptor induced nitric oxide-dependent vasorelaxation.

2017

The Mas receptor is involved in the angiotensin (Ang)-(1-7) vasodilatory actions by increasing nitric oxide production (NO). We have previously demonstrated an increased production of Ang-(1-7) in human umbilical vein endothelial cells (HUVEC) exposed to estradiol (E2), suggesting a potential cross-talk between E2 and the Ang-(1-7)/Mas receptor axis. Here, we explored whether the vasoactive response and NO-related signalling exerted by E2 are influenced by Mas. HUVEC were exposed to 10nM E2 for 24h in the presence or absence of the selective Mas receptor antagonist A779, and the estrogen receptor (ER) antagonist ICI182780 (ICI). E2 increased Akt and endothelial nitric oxide synthase (eNOS) …

0301 basic medicineMalemedicine.medical_specialtyEstrogen receptorVasodilationNitric OxideBiochemistryProto-Oncogene MasUmbilical veinNitric oxideReceptors G-Protein-Coupled03 medical and health scienceschemistry.chemical_compoundMiceEnosInternal medicineProto-Oncogene ProteinsmedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansProtein kinase BPharmacologybiologyAntagonistbiology.organism_classificationMice Inbred C57BLVasodilation030104 developmental biologyEndocrinologychemistryReceptors EstrogenMyographBiochemical pharmacology
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A Network Involving Gut Microbiota, Circulating Bile Acids, and Hepatic Metabolism Genes That Protects Against Non-Alcoholic Fatty Liver Disease.

2019

Scope Gut microbiota contributes to non-alcoholic fatty liver disease (NAFLD) pathogenesis by multiple mechanisms not yet completely understood. Novel differential features between germ-free mice (GFm) transplanted with protective or non-protective cecal microbiota against NAFLD are investigated. Methods and results Gut microbiota composition, plasma, and fecal bile acids (BAs) and liver mRNAs are quantified in GFm recipients from four donor mice differing in NAFLD severity (control diet, high-fat diet [HFD]-responder, HFD-non-responder, and quercetin-supplemented HFD). Transplanted GFm are on control or HFD for 16-weeks. Multivariate analysis shows that GFm colonized with microbiota from H…

0301 basic medicineMalemedicine.medical_specialtyGut floraDiet High-Fatdigestive systemPathogenesisBile Acids and Salts03 medical and health sciencesMiceNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsFeces030109 nutrition & dieteticsbiologyEthanoldigestive oral and skin physiologyFatty livernutritional and metabolic diseasesTransporterbiology.organism_classificationmedicine.diseasePhenotypeGastrointestinal MicrobiomeMice Inbred C57BL030104 developmental biologyEndocrinologyLiverBacteroidesTranscriptomeDrug metabolismFood ScienceBiotechnologyMolecular nutritionfood research
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Neuronal Excitability And Spontaneous Synaptic Transmission In The Entorhinal Cortex Of Bdnf Heterozygous Mice

2018

Abstract Brain Derived Neurotropic Factor (BDNF) is a neutrophic factor that is required for the normal neuronal development and function. BDNF is involved in regulation of synapses as well as neuronal excitability. Entorhinal Cortex (EC) is a key brain area involved in many physiological and pathological processes. In this study we investigated the effects of chronically reduced BDNF levels on layer 3 pyramidal neurons of EC. We aimed to assess the effects of reduced levels of BDNF on firing properties, spontaneous synaptic currents and excitation/inhibition balance from acute brain slices. Patch clamp recordings were obtained from pyramidal neurons of Entorhinal Cortex Layer 3. Findings o…

0301 basic medicineMalemedicine.medical_specialtyHeterozygoteAction potentialAction PotentialsNeurotransmissionInhibitory postsynaptic potentialSynaptic Transmission03 medical and health sciencesMice0302 clinical medicineInternal medicinemedicinePremovement neuronal activityAnimalsEntorhinal CortexPatch clampChemistryGeneral NeuroscienceSpontaneous synaptic transmissionBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsEntorhinal cortex030104 developmental biologyEndocrinologyInhibitory Postsynaptic Potentialsnervous systemGene Knockdown TechniquesExcitatory postsynaptic potentialFemale030217 neurology & neurosurgery
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Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain.

2018

Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodege…

0301 basic medicineMalemedicine.medical_specialtyInflammationmedicine.disease_causeDiet High-FatSettore BIO/09 - FisiologiaNeuroprotectionlcsh:RC321-57103 medical and health sciences0302 clinical medicineNeuroinflammationInternal medicinemedicineGlucagon-Like Peptide 2AnimalsObesityNeurodegenerationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationTUNEL assayGlial fibrillary acidic proteinbiologyChemistryNeurodegenerationdigestive oral and skin physiologyBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyNeuroprotective AgentsNeurologyGliosisOxidative stressAstrocytesbiology.proteinGlucagon-Like Peptide-2 ReceptorOxidative streEncephalitismedicine.symptomInflammation MediatorsGLP-2030217 neurology & neurosurgeryOxidative stresshormones hormone substitutes and hormone antagonistsNeurobiology of disease
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Recombinant human hepatocyte growth factor provides protective effects in cerulein-induced acute pancreatitis in mice.

2018

Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c-Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein-induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip…

0301 basic medicineMalemedicine.medical_specialtyNecrosisPhysiologyClinical BiochemistryInflammationApoptosismedicine.disease_causeProtective AgentsAntioxidantsProinflammatory cytokine03 medical and health sciencesMiceInternal medicineEdemamedicineAnimalsHumansbusiness.industryHepatocyte Growth FactorCell BiologyProto-Oncogene Proteins c-metmedicine.diseaseGlutathioneSurvival AnalysisRecombinant ProteinsDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyPancreatitisAcute pancreatitisPancreatitisHepatocyte growth factormedicine.symptombusinessOxidative stressCeruletidemedicine.drugSignal TransductionJournal of cellular physiology
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Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model.

2019

Traumatic brain injury (TBI) represents a significant risk factor for development of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The S100A9-driven amyloid-neuroinflammatory cascade occurring during primary and secondary TBI events can serve as a mechanistic link between TBI and Alzheimer’s as demonstrated recently in the human brain tissues. Here by using immunohistochemistry in the controlled cortical impact TBI mouse model we have found pro-inflammatory S100A9 in the brain tissues of all mice on the first and third post-TBI days, while 70% of mice did not show any S100A9 presence on seventh post-TBI day similar to controls. This indicates that defensive mechanisms effe…

0301 basic medicineMalemedicine.medical_specialtyNeurologyAmyloidTraumatic brain injuryPlaque AmyloidProtein Aggregation PathologicalS100A9Proinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsCalgranulin BSignificant riskNeuroinflammationNeuronsbusiness.industryGeneral NeuroscienceBrainmedicine.diseasenervous system diseasesDisease Models Animal030104 developmental biologyMicrogliabusinessAlzheimer’s disease Amyloid Neuroinflammation Oligomerization S100A9 Traumatic brain injuryNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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Loop diuretics decrease the renal elimination rate and increase the plasma levels of trimethylamine‐N‐oxide

2018

Aims Trimethylamine-N-oxide (TMAO) is a novel cardiovascular risk marker. We explored the association of commonly used cardiovascular medications with TMAO levels in patients and validated the identified associations in mice. Methods Detailed history of drug treatment was recorded in 300 patients with cardiovascular disease without diabetes in an observational, cross-sectional study. Animal study was performed in CD1 mice. Results Median plasma TMAO (interquartile range) level was 2.144 (1.570-3.104) μmol l-1 . Among nine cardiovascular drug groups, the use of loop diuretics (0.510 ± 0.296 in users vs. 0.336 ± 0.272 in nonusers, P = 0.008) and mineralocorticoid receptor antagonists (0.482 ±…

0301 basic medicineMalemedicine.medical_specialtyOrganic anion transporter 1medicine.drug_classTrimethylamine N-oxide030204 cardiovascular system & hematologyKidneyExcretion03 medical and health scienceschemistry.chemical_compoundMethylaminesMice0302 clinical medicineSodium Potassium Chloride Symporter InhibitorsInternal medicineBlood plasmamedicineAnimalsHumansPharmacology (medical)AgedPharmacologybiologyChemistryArea under the curveFurosemideCardiovascular AgentsHeartOriginal ArticlesLoop diureticMiddle AgedProbenecid030104 developmental biologyEndocrinologyCross-Sectional StudiesLiverCardiovascular Diseasesbiology.proteinFemaleBiomarkersmedicine.drug
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Overactivation of the endocannabinoid system alters the antilipolytic action of insulin in mouse adipose tissue.

2017

Evidence has accumulated that obesity-related metabolic dysregulation is associated with overactivation of the endocannabinoid system (ECS), which involves cannabinoid receptor 1 (CB1R), in peripheral tissues, including adipose tissue (AT). The functional consequences of CB1R activation on AT metabolism remain unclear. Since excess fat mobilization is considered an important primary event contributing to the onset of insulin resistance, we combined in vivo and in vitro experiments to investigate whether activation of ECS could alter the lipolytic rate. For this purpose, the appearance of plasma glycerol was measured in wild-type and CB1R−/− mice after acute anandamide administration or inh…

0301 basic medicineMalemedicine.medical_specialtyPhysiologyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentAdipose tissue030209 endocrinology & metabolismBiologyFatty Acids NonesterifiedCANNABINOID RECEPTOR 103 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineInsulin resistanceDownregulation and upregulationReceptor Cannabinoid CB1Physiology (medical)Internal medicineinsulin resistancemedicineLipolysisAnimalsInsulinendocannabinoid systemInsulinHydrolysis[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismmedicine.diseaseEndocannabinoid systemUp-RegulationJZL195Mice Inbred C57BLcannabinoid receptor 1030104 developmental biologyEndocrinologychemistryAdipose TissuelipolysisJZL195Endocannabinoids
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Age-related regulation of bone formation by the sympathetic cannabinoid CB1 receptor.

2017

The endocannabinoid (eCB) system, including its receptors, ligands, and their metabolizing enzymes, plays an important role in bone physiology. Skeletal cannabinoid type 1 (CB1) receptor signaling transmits retrograde signals that restrain norepinephrine (NE) release, thus transiently stimulating bone formation following an acute challenge, suggesting a feedback circuit between sympathetic nerve terminals and osteoblasts. To assess the effect of chronic in vivo occurrence of this circuit, we characterized the skeletal phenotype of mice with a conditional deletion of the CB1 receptor in adrenergic/noradrenergic cells, including sympathetic nerves. Whereas the deletion of the CB1 receptor did…

0301 basic medicineMalemedicine.medical_specialtySympathetic nervous systemAgingHistologyCannabinoid receptorSympathetic Nervous SystemPhysiologyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentDopamine beta-HydroxylaseBone resorptionBone remodeling03 medical and health sciencesNorepinephrineNorepinephrineReceptor Cannabinoid CB1OsteogenesisInternal medicinemedicineAnimalsNeuropeptide YBone ResorptionReceptorMice KnockoutChemistryEndocannabinoid systemMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyCannabinoidReceptors Adrenergic beta-2Gene Deletionmedicine.drugEndocannabinoidsBone
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Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
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