Search results for "Protection"

showing 10 items of 1623 documents

The cyto-protective effects of LH on ovarian reserve and female fertility during exposure to gonadotoxic alkylating agents in an adult mouse model.

2021

Abstract STUDY QUESTION Does LH protect mouse oocytes and female fertility from alkylating chemotherapy? SUMMARY ANSWER LH treatment before and during chemotherapy prevents detrimental effects on follicles and reproductive lifespan. WHAT IS KNOWN ALREADY Chemotherapies can damage the ovary, resulting in premature ovarian failure and reduced fertility in cancer survivors. LH was recently suggested to protect prepubertal mouse follicles from chemotoxic effects of cisplatin treatment. STUDY DESIGN, SIZE, DURATION This experimental study investigated LH effects on primordial follicles exposed to chemotherapy. Seven-week-old CD-1 female mice were randomly allocated to four experimental groups: C…

0301 basic medicineLHAlkylating Agentsfertility preservationmedia_common.quotation_subjectDNA repair LH cancer chemotherapy fertility preservation follicle protection ovoprotectionDNA repairOvaryMice SCIDBiologychemotherapyAndrology03 medical and health sciencesMice0302 clinical medicineOvarian FollicleMice Inbred NODPregnancyFollicular phasemedicineAnimalsHumanscancerFertility preservationOvarian follicleOvarian reserveOvarian ReserveOvulationmedia_commonReproductive Biology030219 obstetrics & reproductive medicineRehabilitationObstetrics and GynecologyOriginal ArticlesOocytemedicine.diseaseAcademicSubjects/MED00905Premature ovarian failure030104 developmental biologymedicine.anatomical_structureReproductive Medicinefollicle protectionovoprotectionlipids (amino acids peptides and proteins)FemaleHuman reproduction (Oxford, England)
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Medicinal Plants and Natural Products as Potential Sources for Antiparkinson Drugs

2016

Parkinsonʼs disease is a progressive neurodegenerative dysfunction characterized by the loss of pigmented dopaminergic neurons of the nigrostriatal system with a consequent dopamine decrease. The reduction of dopamine levels produces neuronal damage, depigmentation of the substantia nigra, and the presence of intracellular inclusions in dopaminergic neurons. Treatments for Parkinsonʼs disease aim for improving these motor symptoms by increasing the dopaminergic signal in the striatum with levodopa in combination with enzyme inhibitors or anticholinergic drugs. Nevertheless, natural products can act as neuroprotective agents by reducing the progression of the disease and the inflammatory pro…

0301 basic medicineLevodopaPharmaceutical ScienceSubstantia nigraPharmacologyBiologyNeuroprotectionAnalytical ChemistryAntiparkinson Agents03 medical and health sciences0302 clinical medicineDopamineDrug DiscoverymedicineAnimalsHumansPharmacologyBiological ProductsPlants MedicinalPlant ExtractsOrganic ChemistryDopaminergicAntiparkinsonian AgentAntiparkinson drug030104 developmental biologynervous systemComplementary and alternative medicineAntiparkinson AgentsMolecular Medicine030217 neurology & neurosurgeryPhytotherapymedicine.drugPlanta Medica
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Molecular mechanisms underlying the neuroprotective role of atrial natriuretic peptide in experimental acute ischemic stroke

2018

Abstract Along with its role in regulating blood pressure and fluid homeostasis, the natriuretic peptide system could be also part of an endogenous protective mechanism against brain damage. We aimed to assess the possibility that exogenous atrial natriuretic peptide (ANP) could protect against acute ischemic stroke, as well as the molecular mechanisms involved. Three groups of rats subjected to transient middle cerebral artery occlusion (tMCAO, intraluminal filament technique, 60 min) received intracerebroventricular vehicle, low-dose ANP (0.5 nmol) or high-dose ANP (2.5 nmol), at 30 min reperfusion. Neurofunctional condition, and brain infarct and edema volumes were measured at 24 h after…

0301 basic medicineMAPK/ERK pathwayMalePotassium ChannelsSignaling pathwaysmedicine.drug_classMAP Kinase Signaling SystemAcute ischemic strokeDown-RegulationApoptosisBrain damagePharmacologyBiochemistryNeuroprotectionBrain Ischemia03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineEndocrinologyAtrial natriuretic peptideNatriuretic peptideMedicineAnimalsDNA CleavageRats WistarReceptorAtrial natriuretic peptideMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayInjections Intraventricularbusiness.industryCaspase 3Natriuretic peptide receptorsBrainInfarction Middle Cerebral ArteryStroke030104 developmental biologyNeuroprotective AgentsReperfusion InjuryK+ channelsmedicine.symptombusinessProto-Oncogene Proteins c-aktReceptors Atrial Natriuretic Factor030217 neurology & neurosurgeryAtrial Natriuretic Factorhormones hormone substitutes and hormone antagonists
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Resting-state posterior alpha rhythms are abnormal in subjective memory complaint seniors with preclinical Alzheimer's neuropathology and high educat…

2020

International audience; Cognitive reserve is present in Alzheimer's disease (AD) seniors with high education attainment making them clinically resilient to extended brain neuropathology and neurodegeneration. Here, we tested whether subjective memory complaint (SMC) seniors with AD neuropathology and high education attainment of the prospective INSIGHT-preAD cohort (Paris) may present abnormal eyesclosed resting state posterior electroencephalographic rhythms around individual alpha frequency peak, typically altered in AD patients. The SMC participants negative to amyloid PET AD markers (SMCneg) with high (over low-moderate) education level showed higher posterior alpha 2 power density (pos…

0301 basic medicineMaleAgingpsychology [Alzheimer Disease]alpha rhythms; INSIGHT-preAD study; preclinical Alzheimer's disease (AD); preclinical Alzheimer's neuropathology; resting state EEG rhythms; subjective memory complaint (SMC)physiopathology [Brain]Cohort Studies0302 clinical medicineCognitive ReserveMedicineProspective StudiesCognitive reserveAged 80 and over[SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior4. EducationGeneral NeuroscienceNeurodegenerationdiagnosis [Alzheimer Disease]BrainCognitionElectroencephalographyMagnetic Resonance ImagingAlpha Rhythm[SCCO.PSYC]Cognitive science/PsychologyEducational StatusFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]RestAlpha (ethology)NeuropathologyNeuroprotectionphysiopathology [Alzheimer Disease]03 medical and health sciencesRhythmAlzheimer DiseaseMemoryHumansddc:610AgedResting state fMRIbusiness.industry[SCCO.NEUR]Cognitive science/Neurosciencemedicine.disease030104 developmental biologyphysiology [Rest]Positron-Emission TomographyNeurology (clinical)Geriatrics and GerontologybusinessNeuroscience030217 neurology & neurosurgeryDevelopmental Biology
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Very low doses of muscimol and baclofen ameliorate cognitive deficits and regulate protein expression in the brain of a rat model of streptozocin-ind…

2018

Recent studies devoted to neuroprotection have focused on the role of the gamma-aminobutyric acid (GABA) system in regulating neuroinflammatory processes which play a key role in the neurodegenerative processes observed in Alzheimer's disease (AD) by inducing glial cell overactivation and impairing neurotransmission. Data on the efficacy of classical GABA-A and GABA-B receptor agonists (muscimol and baclofen, respectively) in animal models of AD are not available. Moreover, no published studies have examined the ability of optimal doses of these compounds to prevent neuroinflammation, the alterations in neurotransmission and cognitive deficits. In the present study, we used a non-transgenic…

0301 basic medicineMaleBaclofenGlutamate decarboxylaseSpatial LearningPharmacologyNeuroprotectionStreptozocin03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCognitionGABA receptorSTZAlzheimer DiseaseMemoryGlial Fibrillary Acidic ProteinLearningAnimalsRats WistarNeuroinflammationPharmacologyGlial fibrillary acidic proteinbiologyDose-Response Relationship DrugChemistryGABAA receptorMuscimolBrainRatsDisease Models Animal030104 developmental biologyBaclofennervous systemMuscimolGene Expression RegulationRat model of ADbiology.protein:MEDICINE::Physiology and pharmacology::Pharmacological research [Research Subject Categories]Neuroscience030217 neurology & neurosurgeryEuropean journal of pharmacology
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Significance of chronic toxoplasmosis in epidemiology of road traffic accidents in Russian Federation

2017

Studies carried out in Moscow residents have revealed that the prevalence of chronic toxoplasmosis is very close to those in countries of Eastern and Central Europe. Our findings also demonstrated a statistically significant relationship between the rate of traffic accidents and the seroprevalence of chronic toxoplasmosis in drivers who were held responsible for accidents. The latter was 2.37 times higher in drivers who were involved in road accidents compared with control groups. These results suggest that the consequences of chronic toxoplasmosis (particularly a slower reaction time and decreased concentration) might contribute to the peculiarities of the epidemiology of road traffic acci…

0301 basic medicineMaleCritical Care and Emergency Medicinelcsh:MedicineAntibodies ProtozoanRussiaGeographical LocationsEnvironmental protectionEpidemiologyMedicine and Health SciencesPrevalencePublic and Occupational Healthlcsh:ScienceRoad trafficTrauma MedicineGeographic AreasMultidisciplinaryGeographyTraumatic Injury Risk FactorsAccidents Traffic030108 mycology & parasitologyEuropeGeographyRoad Traffic CollisionsFemaleSafetyTraumatic InjuryToxoplasmosisResearch ArticleUrban Areasmedicine.medical_specialtyAsiaCognitive Neuroscience03 medical and health sciencesEnvironmental healthmedicineParasitic DiseasesReaction TimeSeroprevalenceHumansBehaviorProtozoan InfectionsRoad traffic safetylcsh:RTraffic SafetyBiology and Life Sciencesmedicine.diseaseToxoplasmosis030104 developmental biologyImmunoglobulin MCase-Control StudiesImmunoglobulin GPeople and PlacesChronic DiseaseEarth SciencesCognitive Sciencelcsh:QRussian federationhuman activitiesNeurosciencePLoS ONE
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Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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Dimethyl fumarate treatment after traumatic brain injury prevents depletion of antioxidative brain glutathione and confers neuroprotection.

2017

Dimethyl fumarate (DMF) is an immunomodulatory compound to treat multiple sclerosis and psoriasis with neuroprotective potential. Its mechanism of action involves activation of the antioxidant pathway regulator Nuclear factor erythroid 2-related factor 2 thereby increasing synthesis of the cellular antioxidant glutathione (GSH). The objective of this study was to investigate whether post-traumatic DMF treatment is beneficial after experimental traumatic brain injury (TBI). Adult C57Bl/6 mice were subjected to controlled cortical impact followed by oral administration of DMF (80 mg/kg body weight) or vehicle at 3, 24, 48, and 72 h after the inflicted TBI. At 4 days after lesion (dal), DMF-tr…

0301 basic medicineMaleTraumatic brain injuryDimethyl FumarateBrain damagePharmacologyBlood–brain barrierBiochemistryNeuroprotectionAntioxidantsLesion03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsNeuroinflammationDimethyl fumarateGlutathionemedicine.diseaseGlutathioneNeuroprotectionMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologymedicine.anatomical_structureNeuroprotective AgentsBiochemistrychemistryBlood-Brain Barriermedicine.symptom030217 neurology & neurosurgeryJournal of neurochemistry
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Uric acid treatment after stroke modulates the Krüppel-like factor 2-VEGF-A axis to protect brain endothelial cell functions: Impact of hypertension

2019

Uric acid (UA) is a promising protective treatment in ischaemic stroke, but the precise molecular targets underlying its in vivo beneficial actions remain unclear. High concentrations of UA inhibit angiogenesis of cultured endothelial cells via Krüppel-like factor 2 (KLF)-induced downregulation of vascular endothelial growth factor (VEGF), a pro-angiogenic mediator that is able to increase blood–brain barrier (BBB) permeability in acute stroke. Here, we investigated whether UA treatment after ischaemic stroke protects brain endothelial cell functions and modulates the KLF2-VEGF-A axis. Transient intraluminal middle cerebral artery (MCA) occlusion/reperfusion was induced in adult male sponta…

0301 basic medicineMaleVascular Endothelial Growth Factor AVascular endothelial growth factor-AAngiogenesisBiochemistryRats Inbred WKYAntioxidantschemistry.chemical_compound0302 clinical medicineRats Inbred SHRIschaemic strokeEvans BlueBlood-brain barrierBrainKrüppel-like factor 2Vascular endothelial growth factorEndothelial stem cellStrokeVascular endothelial growth factor Amedicine.anatomical_structureNeuroprotective AgentsTreatment OutcomeBlood-Brain Barrier030220 oncology & carcinogenesisHypertensioncardiovascular systemmedicine.symptommedicine.medical_specialtyKruppel-Like Transcription FactorsBrain damageBlood–brain barrierNeuroprotectionCell Line03 medical and health sciencesDouble-Blind MethodInternal medicinemedicineAnimalsHumanscardiovascular diseasesPharmacologybusiness.industryRatsUric Acid030104 developmental biologyEndocrinologychemistryEndothelium VascularAngiogenesisbusinessBiomarkers
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Neuroprotective potential of antihyperglycemic drug metformin in streptozocin-induced rat model of sporadic Alzheimer's disease.

2020

Abstract The earliest hallmarks of sporadic Alzheimer's disease (sAD) are impaired glucose metabolism, chronic neuroinflammation, diminished synaptic plasticity and subsequent cognitive decline. The safest antidiabetic drug metformin has shown both glucose metabolism-improving and cognition-enhancing action in type 2 diabetes patients and diabetic model animals. However, metformin has not been previously studied in intracerebroventricular streptozocin (STZ)-induced model of sAD. Therefore, our aim was to assess the preventive action of metformin in sAD model-rats. Firstly, the actions of metformin (75 and 100 mg/kg) on cognitive functions and sociability were examined. Secondly, we wanted t…

0301 basic medicineMaleendocrine system diseasesNerve Tissue ProteinsType 2 diabetesPharmacologyGPI-Linked ProteinsNeuroprotectionStreptozocin03 medical and health sciencesGlycogen Synthase Kinase 30302 clinical medicineCognitionAlzheimer DiseaseMorris Water Maze TestMedicineAnimalsHypoglycemic AgentsCognitive declineRats WistarSocial BehaviorNeuroinflammationInjections IntraventricularPharmacologyGlucose Transporter Type 1Behavior AnimalGlucose Transporter Type 3business.industrydigestive oral and skin physiologyGlucose transporternutritional and metabolic diseasesBrainmedicine.diseaseMetforminMetforminAstrogliosisDisease Models Animal030104 developmental biologyGlucoseNeuroprotective AgentsSynaptic plasticityAcetylcholinesterasebusinessNeuroglia030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
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