Search results for "STRESS"

showing 10 items of 6278 documents

Anxiolytic effects of muscarinic acetylcholine receptors agonist oxotremorine in chronically stressed rats and related changes in BDNF and FGF2 level…

2017

Rationale: In depressive disorders, one of the mechanisms proposed for antidepressant drugs is the enhancement of synaptic plasticity in the hippocampus and cerebral cortex. Previously, we showed that the muscarinic acetylcholine receptor (mAChR) agonist oxotremorine (Oxo) increases neuronal plasticity in hippocampal neurons via FGFR1 transactivation. Objectives: Here, we aimed to explore (a) whether Oxo exerts anxiolytic effect in the rat model of anxiety-depression-like behavior induced by chronic restraint stress (CRS), and (b) if the anxiolytic effect of Oxo is associated with the modulation of neurotrophic factors, brain-derived neurotrophic factor (BDNF) and fibroblast growth factor-2…

0301 basic medicineMalemedicine.medical_specialtyElevated plus mazemedicine.drug_classBehavioral testPrefrontal CortexHippocampal formationAnxietyMuscarinic AgonistsAnxiolyticHippocampus03 medical and health sciences0302 clinical medicineInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineMuscarinic acetylcholine receptor M4AnimalsElevated plus maze testRats WistarPrefrontal cortexmAChRChronic restraint streForced swimming testPharmacologyNeuronsChemistryBrain-Derived Neurotrophic FactorOxotremorineCerebral cortexRats030104 developmental biologymedicine.anatomical_structureEndocrinologyAnti-Anxiety AgentsCerebral cortexFibroblast Growth Factor 2Anxiety; Behavioral test; Cerebral cortex; Chronic restraint stress; Elevated plus maze test; Forced swimming test; mAChR; Neurotrophins; Novelty suppressed feeding test; PharmacologyNeurotrophinNovelty suppressed feeding testNeuroscience030217 neurology & neurosurgeryStress Psychologicalmedicine.drugPsychopharmacology
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Altered Semmes–Weinstein monofilament test results are associated with oxidative stress markers in type 2 diabetic subjects

2017

Abstract Background Different lines of evidence suggest that oxidative stress (OS) is implicated in the pathogenesis of diabetic neuropathy. The Semmes–Weinstein monofilament (SWM) test is an efficient tool for evaluating diabetic polyneuropathy and diabetic foot. In this study, we analyzed the association between OS markers and altered SWM test results in type 2 diabetes (T2DM) patients. Methods Seventy T2DM patients were studied and 34 showed altered SWM results. The clinical and biochemical parameters were determined using standardized methods. Levels of oxidized glutathione (GSSG) and malondialdehyde (MDA) were measured in circulating mononuclear cells using high-performance liquid chro…

0301 basic medicineMalemedicine.medical_specialtyGlutathione systemDiabetic neuropathySemmes–Weinstein monofilament testlcsh:MedicineType 2 diabetesmedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineMalondialdehydeType 2 diabetes mellitusmedicinePeripheral polyneuropathyHumansAgedAnthropometryGlutathione Disulfidebusiness.industryResearchlcsh:RGeneral Medicinemedicine.diseaseMalondialdehydeDiabetic footHealthy VolunteersOxidative Stress030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2Glutathione disulfideFemaleHemoglobinbusinessPolyneuropathy030217 neurology & neurosurgeryOxidative stressBiomarkersJournal of Translational Medicine
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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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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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Endothelial GLP-1 (Glucagon-Like Peptide 1) Receptor Mediates Cardiovascular Protection by Liraglutide In Mice With Experimental Arterial Hypertension

2019

Supplemental Digital Content is available in the text.

0301 basic medicineMalemedicine.medical_specialtyhypertensionBlotting WesternInflammationBlood Pressure030204 cardiovascular system & hematologyangiotensin IImedicine.disease_causeGlucagon-Like Peptide-1 Receptor1005403 medical and health sciencesMice0302 clinical medicine10030Internal medicinemedicineoxidative stressAnimalsHypoglycemic AgentsReceptor10111Cells CulturedMice KnockoutliraglutideLiraglutidebusiness.industryBasic SciencesType 2 Diabetes MellitusEndothelial CellsAtherosclerosisGlucagon-like peptide-1Angiotensin II3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology10040inflammationComputingMethodologies_DOCUMENTANDTEXTPROCESSINGRNAmedicine.symptomCardiology and Cardiovascular Medicinebusiness10024Oxidative stressmedicine.drug
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Indomethacin counteracts the effects of chronic social defeat stress on emotional but not recognition memory in mice

2017

We have previously observed the impairing effects of chronic social defeat stress (CSDS) on emotional memory in mice. Given the relation between stress and inflammatory processes, we sought to study the effectiveness of the anti-inflammatory indomethacin in reversing the detrimental effects of CSDS on emotional memory in mice. The effects of CSDS and indomethacin on recognition memory were also evaluated. Male CD1 mice were randomly divided into four groups: non-stressed + saline (NS+SAL); non-stressed + indomethacin (NS+IND); stressed + saline (S+SAL); and stressed + indomethacin (S+IND). Stressed animals were exposed to a daily 10 min agonistic confrontation (CSDS) for 20 days. All subjec…

0301 basic medicineMalemedicine.medical_treatmentEmotionsIndomethacinlcsh:MedicineSocial SciencesAnxietySocial defeatMice0302 clinical medicineCognitionLearning and MemoryMedicine and Health SciencesPsychologylcsh:ScienceSalineObject RecognitionMammalsCognitive ImpairmentMultidisciplinaryAnimal BehaviorBehavior AnimalCognitive NeurologyAnti-Inflammatory Agents Non-SteroidalNeurologyAnimal SocialityVertebratesAnxietymedicine.symptomResearch ArticleElevated plus mazemedicine.medical_specialtyCognitive NeurosciencePsychological StressRodents03 medical and health sciencesEmotionalityMemoryInternal medicineMental Health and PsychiatrymedicineAvoidance LearningMemory impairmentAnimalsInterpersonal RelationsRecognition memorySocial stressBehaviorbusiness.industrylcsh:RCognitive PsychologyOrganismsBiology and Life SciencesDisease Models Animal030104 developmental biologyEndocrinologyAmniotesChronic DiseaseCognitive Sciencelcsh:QPerceptionbusinessZoology030217 neurology & neurosurgeryStress PsychologicalNeurosciencePLoS ONE
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Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia

2017

Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated me…

0301 basic medicineMalememoriaAginggenetics [Stress Disorders Post-Traumatic]Diseasegenetics [Neuronal Plasticity]BioinformaticsdemenciaStress Disorders Post-TraumaticMice0302 clinical medicineRisk FactorsNews & ViewsAge of OnsetMice KnockoutNeuronal PlasticitybiologyGeneral NeuroscienceMicrofilament ProteinsNuclear Proteinsgenetics [Nuclear Proteins]FearadultoMiddle AgedAlzheimer's diseasephysiology [Aging]Phenotype3. Good healthPhenotypemiedoFormin 2Forminsgenetics [Aging]estres postraumaticoepidemiology [Stress Disorders Post-Traumatic]AdultHDAC inhibidorpsychology [Dementia]alzheimerForminsNerve Tissue Proteinsepidemiology [Dementia]Affect (psychology)General Biochemistry Genetics and Molecular Biology03 medical and health sciencesHDAC inhibitorMemorygenetics [Dementia]ddc:570medicineDementiaAnimalsHumansenvejecimientoMolecular Biologyphysiology [Memory]General Immunology and MicrobiologyPost-traumatic stress disordermedicine.diseaseYoung age030104 developmental biologyformin 2 protein mouseCase-Control StudiesSynaptic plasticitybiology.proteinDementiagenetics [Microfilament Proteins]complications [Stress Disorders Post-Traumatic]030217 neurology & neurosurgeryHomeostasis
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Mismatch or allostatic load? Timing of life adversity differentially shapes gray matter volume and anxious temperament

2015

Traditionally, adversity was defined as the accumulation of environmental events (allostatic load). Recently however, a mismatch between the early and the later (adult) environment (mismatch) has been hypothesized to be critical for disease development, a hypothesis that has not yet been tested explicitly in humans. We explored the impact of timing of life adversity (childhood and past year) on anxiety and depression levels (N = 833) and brain morphology (N = 129). Both remote (childhood) and proximal (recent) adversities were differentially mirrored in morphometric changes in areas critically involved in emotional processing (i.e. amygdala/hippocampus, dorsal anterior cingulate cortex, res…

0301 basic medicineMalestressful life eventschildhood maltreatmentEmotionsAnxietySocial EnvironmentDevelopmental psychology0302 clinical medicineGray MatterVBMChildadversitymedia_commonDepressionAdult Survivors of Child AbuseAllostasisBrainGeneral MedicineOrgan SizeMagnetic Resonance ImagingAllostatic loadmedicine.anatomical_structureAllostasisAnxietyFemalemedicine.symptomPsychologymismatchallostatic loadAdultCognitive Neurosciencemedia_common.quotation_subjectExperimental and Cognitive PsychologyAffect (psychology)AmygdalaLife Change Events03 medical and health sciencesYoung AdultmedicineHumansddc:610TemperamentAnterior cingulate cortexBrain morphometryOriginal ArticlesImage Enhancement030104 developmental biologyTemperament030217 neurology & neurosurgerySocial Cognitive and Affective Neuroscience
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Redox-related biomarkers in physical exercise

2021

Research in redox biology of exercise has made considerable advances in the last 70 years. Since the seminal study of George Pake's group calculating the content of free radicals in skeletal muscle in resting conditions in 1954, many discoveries have been made in the field. The first section of this review is devoted to highlight the main research findings and fundamental changes in the exercise redox biology discipline. It includes: i) the first steps in free radical research, ii) the relation between exercise and oxidative damage, iii) the redox regulation of muscle fatigue, iv) the sources of free radicals during muscle contractions, and v) the role of reactive oxygen species as regulato…

0301 basic medicineMedicine (General)QH301-705.5Clinical BiochemistryPopulationPhysical exerciseBioinformaticsmedicine.disease_causeBiochemistryRedoxAntioxidants03 medical and health sciences0302 clinical medicineR5-920Free radicalmedicineBiology (General)educationMuscle SkeletalExerciseeducation.field_of_studyMuscle fatigueOvertrainingOrganic ChemistryArticles from the Special Issue on Oxidative stress in retina and retinal pigment epithelium in health and disease; Edited by Dr. Vera BonilhaSkeletal musclemedicine.disease030104 developmental biologymedicine.anatomical_structureOxidative stressBiomarker (medicine)Reactive Oxygen SpeciesOxidation-Reduction030217 neurology & neurosurgeryOxidative stressBiomarkersRedox Biology
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