Search results for "Protection"

showing 10 items of 1623 documents

Hypoxia in CNS Pathologies: Emerging Role of miRNA-Based Neurotherapeutics and Yoga Based Alternative Therapies

2017

Cellular respiration is a vital process for the existence of life. Any condition that results in deprivation of oxygen (also termed as hypoxia) may eventually lead to deleterious effects on the functioning of tissues. Brain being the highest consumer of oxygen is prone to increased risk of hypoxia-induced neurological insults. This in turn has been associated with many diseases of central nervous system (CNS) such as stroke, Alzheimer's, encephalopathy etc. Although several studies have investigated the pathophysiological mechanisms underlying ischemic/hypoxic CNS diseases, the knowledge about protective therapeutic strategies to ameliorate the affected neuronal cells is meager. This has au…

0301 basic medicineEncephalopathyCentral nervous systemIschemiaReviewischemiaBiologyNeuroprotectionlcsh:RC321-571breathing exercise03 medical and health sciencesTherapeutic approach0302 clinical medicinemicroRNAmedicineGene silencinglcsh:Neurosciences. Biological psychiatry. NeuropsychiatrymicroRNAhypoxiaGeneral NeuroscienceHypoxia (medical)medicine.disease030104 developmental biologymedicine.anatomical_structureyoganeuroprotectionmedicine.symptomNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Neuroscience
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Prevention of an increase in cortical ligand binding to AMPA receptors may represent a novel mechanism of endogenous brain protection by G-CSF after …

2016

PURPOSE Using G-CSF deficient mice we recently demonstrated neuroprotective properties of endogenous G-CSF after ischemic stroke. The present follow-up study was designed to check, whether specific alterations in ligand binding densities of excitatory glutamate or inhibitory GABAA receptors may participate in this effect. METHODS Three groups of female mice were subjected to 45 minutes of MCAO: wildtype, G-CSF deficient and G-CSF deficient mice substituted with G-CSF. Infarct volumes were determined after 24 hours and quantitative in vitro receptor autoradiography was performed using [3H]MK-801, [3H]AMPA and [3H]muscimol for labeling of NMDA, AMPA and GABAA receptors, respectively. Ligand b…

0301 basic medicineExcitotoxicityAMPA receptorPharmacologymedicine.disease_causeReceptors N-Methyl-D-AspartateNeuroprotectionBrain IschemiaMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDevelopmental NeuroscienceGranulocyte Colony-Stimulating FactormedicineAnimalsReceptors AMPAReceptorGABAA receptorGlutamate receptorReceptors GABA-ANeuroprotectionStroke030104 developmental biologynervous systemNeurologyMuscimolchemistryAutoradiographyNMDA receptorFemaleNeurology (clinical)030217 neurology & neurosurgeryRestorative Neurology and Neuroscience
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ADAM10 in Alzheimer's disease: Pharmacological modulation by natural compounds and its role as a peripheral marker.

2019

Abstract Alzheimer’s disease (AD) represents a global burden in the economics of healthcare systems. Amyloid-β (Aβ) peptides are formed by amyloid-β precursor protein (AβPP) cleavage, which can be processed by two pathways. The cleavage by the α-secretase A Disintegrin And Metalloprotease 10 (ADAM10) releases the soluble portion (sAβPPα) and prevents senile plaques. This pathway remains largely unknown and ignored, mainly regarding pharmacological approaches that may act via different signaling cascades and thus stimulate non-amyloidogenic cleavage through ADAM10. This review emphasizes the effects of natural compounds on ADAM10 modulation, which eventuates in a neuroprotective mechanism. M…

0301 basic medicineFarmacologiaADAM10DiseaseRM1-950Natural compoundsCleavage (embryo)NeuroprotectionCatechin03 medical and health sciencesADAM10 ProteinAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseDisintegrinHumansSenile plaquesPharmacological modulationPharmacologyMetalloproteinaseAmyloid beta-PeptidesbiologyChemistryPlant ExtractsADAM10ProteinsGinkgo bilobaMembrane ProteinsGeneral Medicineα-SecretaseAlzheimer's disease030104 developmental biologyMalaltia d'AlzheimerNeuroprotective Agents030220 oncology & carcinogenesisPharmaceuticalbiology.proteinTherapeutics. PharmacologyAmyloid Precursor Protein SecretasesNeuroscienceAlzheimer’s diseaseProteïnesBiomarkersBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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Enhancement in Phospholipase D Activity as a New Proposed Molecular Mechanism of Haloperidol-Induced Neurotoxicity

2020

Membrane phospholipase D (PLD) is associated with numerous neuronal functions, such as axonal growth, synaptogenesis, formation of secretory vesicles, neurodegeneration, and apoptosis. PLD acts mainly on phosphatidylcholine, from which phosphatidic acid (PA) and choline are formed. In turn, PA is a key element of the PLD-dependent secondary messenger system. Changes in PLD activity are associated with the mechanism of action of olanzapine, an atypical antipsychotic. The aim of the present study was to assess the effect of short-term administration of the first-generation antipsychotic drugs haloperidol, chlorpromazine, and fluphenazine on membrane PLD activity in the rat brain. Animals were…

0301 basic medicineFluphenazineolanzapinePhospholipasePharmacologyCatalysishaloperidollcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineneurotoxicityHaloperidolmedicineAnimalsphospholipase DPhospholipase D activityPhysical and Theoretical ChemistryChlorpromazinechlorpromazinelcsh:QH301-705.5Molecular BiologySpectroscopy030102 biochemistry & molecular biologyPhospholipase DCommunicationOrganic ChemistryGeneral MedicinePhosphatidic acidfluphenazineRatsComputer Science ApplicationsEnzyme Activationenzymes and coenzymes (carbohydrates)lcsh:Biology (General)lcsh:QD1-999chemistryMechanism of actionneuroprotectionlipids (amino acids peptides and proteins)medicine.symptom030217 neurology & neurosurgerymedicine.drugInternational Journal of Molecular Sciences
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Atypical 1,4-dihydropyridine derivatives, an approach to neuroprotection and memory enhancement

2016

This mini review is devoted to the design and pharmacological studies of novel atypical 1,4-dihydropyridine (DHP) derivatives which differ to a great extent from the traditional DHPs either by lack of neuronal calcium channel blocking activity and/or inability to protect mitochondrial processes. About 100 new DHP derivatives were screened and the mostly active were selected for detailed studies. The compounds of the series of the amino acid ("free" plus "crypto")-containing DHPs and lipophilic di-cyclic DHPs demonstrated long-lasting neuroprotective and/or memory-enhancing action, particularly at low doses (0.005-0.05mg/kg) in different neurodeficiency rat or mice models, and exerted neurot…

0301 basic medicineGenetically modified mouseDihydropyridinesDHPSNeurotransmissionBiologyPharmacologyNeuroprotection03 medical and health sciences0302 clinical medicineMemoryAnimalsHumansPharmacologychemistry.chemical_classificationNeurotransmitter AgentsCalcium channelCalcium Channel BlockersNeuroprotectionAmino acid030104 developmental biologychemistrySynaptic plasticityNervous System DiseasesNeurotransmitter AgentsNeuroscience030217 neurology & neurosurgeryPharmacological Research
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Autoimmune aspects in glaucoma

2016

The pathogenesis of glaucoma, a common neurodegenerative disease, involves an immunologic component. Studies demonstrate changes of autoantibody concentrations against retinal and optic nerve head antigens in glaucoma patients. Furthermore we found antibody deposits in human glaucomatous retinae in a pro-inflammatory environment. Clinical studies showed up regulated, but also significantly down-regulated autoantibody levels. These antibodies belong to the natural autoimmunity. The upregulation of autoantibodies can be associated with fatal conditions, but several studies demonstrate that natural autoantibodies entail also neuroprotective characteristics and influence the protein expression …

0301 basic medicineGlaucomaAutoimmunityDiseasemedicine.disease_causeNeuroprotectionAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicineAntigenmedicineAnimalsHumansAutoantibodiesPharmacologybusiness.industryAutoantibodyGlaucomamedicine.diseaseNeuroprotection030104 developmental biologyImmunology030221 ophthalmology & optometryBiomarker (medicine)sense organsbusinessEuropean Journal of Pharmacology
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Insecticidal spectrum and mode of action of the Bacillus thuringiensis Vip3Ca insecticidal protein.

2016

The Vip3Ca protein, discovered in a screening of Spanish collections of Bacillus thuringiensis, was known to be toxic to Chrysodeixis chalcites, Mamestra brassicae and Trichoplusia ni. In the present study, its activity has been tested with additional insect species and we found that Cydia pomonella is moderately susceptible to this protein. Vip3Ca (of approximately 90 kDa) was processed to an approximately 70 kDa protein when incubated with midgut juice in all tested species. The kinetics of proteolysis correlated with the susceptibility of the insect species to Vip3Ca. The activation was faster to slower in the following order: M. brassicae (susceptible), Spodoptera littoralis (moderately…

0301 basic medicineInsecticides030106 microbiologyInsect pest controlAgrotis ipsilonVegetative insecticidal proteinsMothsmedicine.disease_causeMicrobiologyCiencias BiológicasInsecticide Resistance03 medical and health sciencesBiología Celular MicrobiologíaBacterial ProteinsBacillus thuringiensisBotanyTrichoplusiamedicineAnimalsSpodoptera littoralisPest Control BiologicalEcology Evolution Behavior and SystematicsHistological localizationbiologyToxinfungiVEGETATIVE INSECTICIDAL PROTEINSMidgutBioinsecticidesApical membranebiology.organism_classificationCROP PROTECTIONChrysodeixis chalcitesBIOINSECTICIDES030104 developmental biologyCrop protectionINSECT PEST CONTROLHISTOLOGICAL LOCALIZATIONCIENCIAS NATURALES Y EXACTASJournal of invertebrate pathology
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A Genomic and Proteomic Approach to Identify and Quantify the Expressed Bacillus thuringiensis Proteins in the Supernatant and Parasporal Crystal

2018

The combined analysis of genomic and proteomic data allowed us to determine which cry and vip genes are present in a Bacillus thuringiensis (Bt) isolate and which ones are being expressed. Nine Bt isolates were selected from Spanish collections of Bt based on their vip1 and vip2 gene content. As a first step, nine isolates were analyzed by PCR to select those Bt isolates that contained genes with the lowest similarity to already described vip1 and vip2 genes (isolates E-SE10.2 and O-V84.2). Two selected isolates were subjected to a combined genomic and proteomic analysis. The results showed that the Bt isolate E-SE10.2 codifies for two new vegetative proteins, Vip2Ac-like_1 and Sip1Aa-like_…

0301 basic medicineInsecticidesbiologyInsect pest controlHealth Toxicology and MutagenesisSingle typelcsh:Rcry proteinslcsh:Medicinevip proteinsToxicologybiology.organism_classificationMolecular biologyinsect pest control; crop protection; vip proteins; cry proteins03 medical and health sciences030104 developmental biologyinsect pest controlBacillus thuringiensisGeneProteïnescrop protection
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Neuroprotective and Anti-Inflammatory Effects of a Hydrophilic Saffron Extract in a Model of Glaucoma

2019

Glaucoma is a neurodegenerative disease characterized by the loss of retinal ganglion cells (RGCs). An increase in the intraocular pressure is the principal risk factor for such loss, but controlling this pressure does not always prevent glaucomatous damage. Activation of immune cells resident in the retina (microglia) may contribute to RGC death. Thus, a substance with anti-inflammatory activity may protect against RGC degeneration. This study investigated the neuroprotective and anti-inflammatory effects of a hydrophilic saffron extract standardized to 3% crocin content in a mouse model of unilateral, laser-induced ocular hypertension (OHT). Treatment with saffron extract decreased microg…

0301 basic medicineIntraocular pressureretinagenetic structuresAnti-Inflammatory AgentsOcular hypertensionmicrogliaPharmacologysaffron extractneuroinflammationCrocinlcsh:ChemistryMicechemistry.chemical_compound0302 clinical medicinelcsh:QH301-705.5SpectroscopyIba-1General MedicineComputer Science ApplicationsNeuroprotective Agentsmedicine.anatomical_structureRetinal ganglion cellOftalmologíaneuroprotectionHydrophobic and Hydrophilic InteractionsNeurocienciasRetinal ganglionNeuroprotectionArticleCatalysisganglion cellsInorganic Chemistry03 medical and health sciencesP2RY12medicineAnimalsPhysical and Theoretical ChemistryMolecular BiologyIntraocular PressureNeuroinflammationexperimental glaucomaRetinaPlant Extractsbusiness.industryOrganic ChemistryBrn3aGlaucomaCrocusmedicine.diseaseAnatomía oculareye diseasesDisease Models Animal030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999sense organsbusinessBiomarkers030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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In vivo and in vitro effects of multiple sclerosis immunomodulatory therapeutics on glutamatergic excitotoxicity.

2015

In multiple sclerosis (MS), a candidate downstream mechanism for neuronal injury is glutamate (Glu)-induced excitotoxicity, leading to toxic increases in intraneuronal Ca(2+) . Here, we used in vivo two-photon imaging in the brain of TN-XXL transgenic Ca(2+) reporter mice to test whether promising oral MS therapeutics, namely fingolimod, dimethyl fumarate, and their respective metabolites fingolimod-phosphate and monomethyl fumarate, can protect neurons against acute glutamatergic excitotoxic damage. We also assessed whether these drugs can protect against excitotoxicity in vitro using primary cortical neurons, and whether they can directly inhibit Glu release from pathogenic T-helper 17 ly…

0301 basic medicineKainic acidMultiple SclerosisExcitotoxicityGlutamic AcidPharmacologyBiologymedicine.disease_causeBiochemistryNeuroprotectionImmunomodulation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineIn vivomedicineAnimalsCells CulturedNeuronsKainic AcidDimethyl fumarateCell DeathGlutamate receptorNeurotoxicityBrainmedicine.diseaseUp-Regulation030104 developmental biologyNeuroprotective AgentschemistryNMDA receptor030217 neurology & neurosurgerySignal TransductionJournal of neurochemistry
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