Search results for "Protection"

showing 10 items of 1623 documents

GABA-containing compound gammapyrone protects against brain impairments in Alzheimer's disease model male rats and prevents mitochondrial dysfunction…

2018

Neuroinflammation, oxidative stress, decreased glucose/energy metabolism, and disrupted neurotransmission are changes that occur early in sporadic Alzheimer's disease (AD), manifesting as mild cognitive impairment. Recently, the imbalanced function of the gamma-aminobutyric acid (GABA) system was identified as a critical factor in AD progression. Thus, maintaining balance among neurotransmitter systems, particularly the GABA system, can be considered a beneficial strategy to slow AD progression. The present study investigated the effects of the compound gammapyrone, a molecule containing three GABA moieties: "free" moiety attached to the position 4 of the 1,4-dihydropyridine (DHP) ring, and…

0301 basic medicineMalemedicine.medical_specialtyAllosteric regulationbioenergetics; GABA; intracerebroventricular streptozocin; PC12 cells; protein expression; spatial learning/memoryNeurotransmissionspatial learning/memorymedicine.disease_causebioenergeticsNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceGABA0302 clinical medicineReceptors GABAAlzheimer DiseaseMemoryInternal medicinemedicineAnimalsRats WistarReceptorMaze Learningprotein expressionNeuroinflammationCells Culturedgamma-Aminobutyric AcidGABAA receptorChemistryGlutamate DecarboxylasePC12 cellsBrainintracerebroventricular streptozocinMitochondriaStreptozocinDisease Models Animal030104 developmental biologyEndocrinologyNeuroprotective AgentsAstrocytesAcetylcholinesteraseEncephalitisMicroglia030217 neurology & neurosurgeryOxidative stressJournal of neuroscience research
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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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Emergent Uric Acid Treatment is Synergistic with Mechanical Recanalization in Improving Stroke Outcomes in Male and Female Rats.

2018

Preclinical and clinical studies support a promising, albeit not definitive, neuroprotective effect of emergent uric acid (UA) administration in ischemic stroke. We assessed the effects of UA in an ischemic stroke model relevant to the current treatment paradigm of mechanical thrombectomy within the STAIR/RIGOR recommendations. A cohort of male and female Wistar rats was subjected to ischemic stroke with mechanical recanalization under physiological monitoring. The effects of transient middle cerebral artery occlusion (tMCAO) with adjunctive UA (IV, 16 mg/kg) or vehicle treatment were assessed at 24 h and 7 days. Outcomes included neurofunctional impairment, brain infarct (TTC staining, MRI…

0301 basic medicineMalemedicine.medical_specialtyMechanical ThrombolysisBrain damageNeuroprotectionBrain Ischemia03 medical and health sciencesCresyl violetchemistry.chemical_compoundRandom Allocation0302 clinical medicineuric acidInternal medicineEdemamedicineischemic strokeAnimalsRats WistarStrokebusiness.industryGeneral Neurosciencerat modeladjunctive treatmentBrainRecovery of Functionmedicine.diseaseCombined Modality TherapyUric AcidStrokeDisease Models Animal030104 developmental biologyNeuroprotective AgentschemistrythrombectomyAdjunctive treatmentIschemic strokeCardiologyUric acidneuroprotectionFemalemedicine.symptombusiness030217 neurology & neurosurgeryNeuroscience
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Sex hormones modulate pathogenic processes in experimental traumatic brain injury.

2018

Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…

0301 basic medicineMalemedicine.medical_specialtyanimal structuresmedicine.drug_classmedicine.medical_treatmentTropomyosin receptor kinase BTropomyosin receptor kinase ABiochemistryNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineInternal medicineBrain Injuries TraumaticmedicineAnimalsNerve Growth FactorsSex CharacteristicsbiologyEstradiolbusiness.industryEstrogen AntagonistsBrainDihydrotestosteroneAndrogennervous system diseasesMice Inbred C57BLSteroid hormoneDisease Models Animal030104 developmental biologyEndocrinologynervous systemSex steroidDihydrotestosteronebiology.proteinFemalebusiness030217 neurology & neurosurgeryNeurotrophinmedicine.drugJournal of neurochemistry
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The Role of NF-κB Triggered Inflammation in Cerebral Ischemia

2021

Cerebral ischemia is a devastating disease that affects many people worldwide every year. The neurodegenerative damage as a consequence of oxygen and energy deprivation, to date, has no known effective treatment. The ischemic insult is followed by an inflammatory response that involves a complex interaction between inflammatory cells and molecules which play a role in the progression towards cell death. However, there is presently a matter of controversy over whether inflammation could either be involved in brain damage or be a necessary part of brain repair. The inflammatory response is triggered by inflammasomes, key multiprotein complexes that promote secretion of pro-inflammatory cytoki…

0301 basic medicineMini ReviewIschemiaNeurosciences. Biological psychiatry. NeuropsychiatryContext (language use)InflammationBrain damageCervell Ferides i lesionsNeuroprotectionNF-κBcerebral ischemia03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicinebusiness.industryNeurodegenerationneurodegenerationNF-κBInflammasomemedicine.disease030104 developmental biologychemistryinflammationCellular Neuroscienceneuroprotectionmedicine.symptombusinessOxigen Efectes fisiològicsNeuroscience030217 neurology & neurosurgeryRC321-571medicine.drugFrontiers in Cellular Neuroscience
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The role of mitochondrial reactive oxygen species, NO and H2S in ischaemia/reperfusion injury and cardioprotection

2020

Redox signalling in mitochondria plays an important role in myocardial ischaemia/reperfusion (I/R) injury and in cardioprotection. Reactive oxygen and nitrogen species (ROS/RNS) modify cellular structures and functions by means of covalent changes in proteins including among others S‐nitros(yl)ation by nitric oxide (NO) and its derivatives, and S‐sulphydration by hydrogen sulphide (H2S). Many enzymes are involved in the mitochondrial formation and handling of ROS, NO and H2S under physiological and pathological conditions. In particular, the balance between formation and removal of reactive species is impaired during I/R favouring their accumulation. Therefore, various interventions aimed a…

0301 basic medicineMitochondrial ROSIschemiaEndogenyheartMitochondrionRedoxNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinenitric oxidemedicinechemistry.chemical_classificationCardioprotectionreactive oxygen speciesReactive oxygen speciesVDP::Medisinske Fag: 700::Basale medisinske odontologiske og veterinærmedisinske fag: 710Cell Biologymedicine.diseaseVDP::Medical disciplines: 700::Basic medical dental and veterinary science disciplines: 710Cell biologyreperfusionmitochondria030104 developmental biologychemistry030220 oncology & carcinogenesiscardioprotectionMolecular Medicineischaemiahydrogen sulphidecardioprotection; heart; hydrogen sulphide; ischaemia; mitochondria; nitric oxide; reactive oxygen species; reperfusion
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Genetically modified seeds and plant propagating material in Europe: potential routes of entrance and current status

2019

Genetically modified organisms (GMO), mainly crop plants, are increasingly grown worldwide leading to large trade volumes of living seeds and other plant material both for cultivation and for food and animal feed. Even though all the traded GMOs have been assessed for their safety with regards to human and animal health and the environment, there still are some concerns regarding the potential uncontrolled release in the environment of authorized or unauthorized GM plants. In this review, we identify the possible entrance routes of GM seeds and other propagating plant material in the EU which could be linked to unauthorized release of GMOs in the environment. In addition, we discuss the sit…

0301 basic medicineMultidisciplinaryAnimal healthAnimal feedbusiness.industryGenetically modified cropsFood safetyPlant cultivationArticleGenetically modified organismFood safety03 medical and health sciences030104 developmental biology0302 clinical medicineEnvironmental protectionlcsh:H1-99Businesslcsh:Social sciences (General)lcsh:Science (General)030217 neurology & neurosurgeryBiotechnologylcsh:Q1-390Heliyon
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Neurodegenerative diseases: Might citrus flavonoids play a protective role?

2016

Neurodegenerative diseases (ND) result from the gradual and progressive degeneration of the structure and function of the central nervous system or the peripheral nervous system or both. They are characterized by deterioration of neurons and/or myelin sheath, disruption of sensory information transmission and loss of movement control. There is no effective treatment for ND, and the drugs currently marketed are symptom-oriented, albeit with several side effects. Within the past decades, several natural remedies have gained attention as potential neuroprotective drugs. Moreover, an increasing number of studies have suggested that dietary intake of vegetables and fruits can prevent or delay th…

0301 basic medicineNervous systemCitrusCitruPharmaceutical ScienceReviewDegeneration (medical)Analytical Chemistry0302 clinical medicineDrug DiscoveryNeuropharmacologyTraditional medicineNeurodegenerationfood and beveragesNeurodegenerative Diseases3. Good healthNeuroprotective Agentsmedicine.anatomical_structureChemistry (miscellaneous)Myelin sheathMolecular MedicineNutraceuticalHumanCitrus; Flavonoids; Neurodegeneration; Neurodegenerative disorders; Nutraceutical; Citrus; Fruit; Humans; Neurodegenerative Diseases; Flavonoids; Neuroprotective Agents; Organic ChemistryNeuroprotective AgentBiologyNeuroprotectionlcsh:QD241-44103 medical and health sciencesNutraceuticallcsh:Organic chemistrySettore MED/43 - Medicina LegalemedicineHumansEffective treatmentPhysical and Theoretical ChemistryNeurodegenerationFlavonoidsNeurodegenerative Diseasebusiness.industryOrganic ChemistryCitrus; Flavonoids; Neurodegeneration; Neurodegenerative disorders; Nutraceutical; Medicine (all);Neurodegenerative disordermedicine.diseaseBiotechnology030104 developmental biologyFruitNeurodegenerative disordersFlavonoidSettore BIO/14 - Farmacologiabusiness030217 neurology & neurosurgery
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Lactate as a Metabolite and a Regulator in the Central Nervous System

2016

More than two hundred years after its discovery, lactate still remains an intriguing molecule. Considered for a long time as a waste product of metabolism and the culprit behind muscular fatigue, it was then recognized as an important fuel for many cells. In particular, in the nervous system, it has been proposed that lactate, released by astrocytes in response to neuronal activation, is taken up by neurons, oxidized to pyruvate and used for synthesizing acetyl-CoA to be used for the tricarboxylic acid cycle. More recently, in addition to this metabolic role, the discovery of a specific receptor prompted a reconsideration of its role, and lactate is now seen as a sort of hormone, even invol…

0301 basic medicineNervous systemlactate transporterCentral nervous systemReviewBiologyBlood–brain barrierlactate receptorsNeuroprotectionCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineSettore BIO/10 - Biochimicalactate receptormedicineAnimalsHumanslactate transportersPhysical and Theoretical ChemistryReceptorExerciselcsh:QH301-705.5Molecular BiologySpectroscopyOrganic ChemistryNeurodegenerationlactic acidBrainGeneral MedicineMetabolismblood-brain barriermedicine.diseaseComputer Science ApplicationsCitric acid cycle030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999Biochemistrybrain metabolismActic acidexercise and lactateEnergy MetabolismNeuroscience030217 neurology & neurosurgerySignal Transductionactic acid; brain metabolism; lactate transporters; blood-brain barrier; lactate receptors; exercise and lactate
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Carnosine protects pancreatic beta cells and islets against oxidative stress damage

2018

Abstract Islet transplantation is a valid therapeutic option for type 1 diabetes treatment. However, in this procedure one of the major problems is the oxidative stress produced during pancreatic islet isolation. The aim of our study was to evaluate potential protective effects of L-carnosine and its isomer D-carnosine against oxidative stress. We evaluated the carnosine effect on cell growth, cell death, insulin production, and the main markers of oxidative stress in rat and murine stressed beta cell lines as well as in human pancreatic islets. Both isomers clearly inhibited hydrogen peroxide induced cytotoxicity, with a decrease in intracellular reactive oxygen and nitrogen species, preve…

0301 basic medicineNitrous OxideCarnosineApoptosismedicine.disease_causeBiochemistrychemistry.chemical_compoundMice0302 clinical medicineEndocrinologyInsulin-Secreting CellsInsulin Secretiongeography.geographical_feature_categoryChemistryNitrotyrosineCarnosineDiabetesIsletReactive Nitrogen Speciesmedicine.anatomical_structureBeta cellPancreatic islet transplantationmedicine.medical_specialtyCell SurvivalProtective AgentsCell Line03 medical and health sciencesInternal medicinemedicineAnimalsHumansMolecular BiologyBeta cell lineCell ShapeCell ProliferationSettore MED/04 - Patologia GeneralegeographyPancreatic isletsTranscription Factor RelAHydrogen PeroxideRatsTransplantationOxidative Stress030104 developmental biologyEndocrinologyGlucoseGene Expression RegulationCytoprotectionTyrosinePancreatic islet transplantationReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressBiomarkers
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