Search results for "Protection"

showing 10 items of 1623 documents

Prevention and Clinical Management of Cardiovascular Damage Induced by Anticancer Drugs: Need gor Early Biomarkers snd Cardio- snd Vasculo-Protection…

2018

The use of chemotherapy has largely improved the prognosis of cancer patients in the past two decades. However, the advent of more effective anticancer therapies has led to a higher incidence of cardiovascular toxicity that shows an increased incidence and represents a significant determinant of quality of life and mortality during ongoing treatment and in long-term survivors of cancer. In this setting, the primary objective for cardiologists and oncologists is the early identification of patients at high risk for developing cardiovascular toxicity and the identification of the cardiovascular cardiotoxicity in the earliest stages to personalize cancer therapy, arrange preventive interventio…

Cardiovascular toxicityCardiotoxicitymedicine.medical_specialtyChemotherapyVascular Toxicitybusiness.industryIncidence (epidemiology)medicine.medical_treatmentBiomarkers Omics Cardioprotection Vasculoprotection Cardiotoxicity Vascular Toxicity Anticancer drugsVasculoprotectionCancerOmicsCardioprotectionmedicine.diseaseOmicsAnticancer drugsCardiotoxicityQuality of lifemedicinePersonalized therapyIntensive care medicinebusinessBiomarkers
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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Central nicotinic receptors, neurotrophic factors and neuroprotection

2000

The multiple combinations of nAChR subunits identified in central nervous structures possess distinct pharmacological and physiological properties. A growing number of data have shown that compounds interacting with neuronal nAChRs have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improving of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's and Parkinson's disease. Taken together experimental and clinical data largely ind…

Cell SurvivalAgonist-antagonistCentral nervous systemReceptors Nicotiniccomplex mixturesNeuroprotectionBehavioral NeuroscienceNeurotrophic factorsmental disordersmedicineAnimalsHumansNerve Growth FactorsAcetylcholine receptorNeuronsRegulation of gene expressionbiologymusculoskeletal neural and ocular physiologyBrainHaplorhinimedicine.diseaseRatsNeuroprotective Agentsmedicine.anatomical_structurenervous systembiology.proteinFibroblast Growth Factor 2sense organsAlzheimer's diseasePsychologyNeuroscienceNeurotrophinBehavioural Brain Research
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Galantamine modulates nicotinic receptor and blocks Aβ-enhanced glutamate toxicity

2004

Galantamine is a plant alkaloid that is used in the treatment of Alzheimer's disease. We have studied the effects of galantamine on beta-amyloid-enhanced glutamate toxicity using primary rat cultured cortical neurons. Nicotine and galantamine alone, and in combination, protected neurons against this neurotoxicity. The protection was not blocked by alpha4beta2 nicotinic acetylcholine receptor (nAChR) antagonists, but was partially blocked by alpha7 nAChR antagonists. Galantamine induced phosphorylation of Akt, an effector of phosphatidylinositol 3-kinase (PI3K), while PI3K inhibitors blocked the protective effect and Akt phosphorylation. The antibody FK1, which selectively blocks the alloste…

Cell SurvivalBiophysicsGlutamic AcidReceptors NicotinicPharmacologycomplex mixturesBiochemistryNeuroprotectionmedicineGalantamineAnimalsDrug InteractionsMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCerebral CortexNeuronsAmyloid beta-PeptidesDose-Response Relationship DrugGalantamineChemistryGlutamate receptorNeurotoxicityCell Biologymedicine.diseaseRatsNeuroprotective AgentsNicotinic agonistnervous systemPhosphorylationmedicine.drugBiochemical and Biophysical Research Communications
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Differential regulation of apoptosis-associated genes by estrogen receptor alpha in human neuroblastoma cells

2012

Purpose: The neuroendocrinology of female sex hormones is of great interest for a variety of neuropsychiatric disorders. In fact, estrogens and estrogen receptors (ERs) exert neuromodulatory and neuroprotective functions. Here we investigated potential targets of the ER subtype alpha that may mediate neuroprotection and focused on direct modulators and downstream executors of apoptosis. Methods: We employed subclones of human neuroblastoma cells (SK-N-MC) stably transfected with one of the ER subtypes, ERalpha or ERbeta. Differences between the cell lines regarding the mRNA expression levels were examined by qPCR, changes on protein levels were examined by Western Blot and immunocytochemist…

Cell SurvivalEstrogen receptorApoptosisCaspase 3BiologyNeuroprotectionRats Sprague-DawleyNeuroblastomaDevelopmental NeuroscienceCell Line TumorAnimalsEstrogen Receptor betaHumansGene silencingAdaptor Proteins Signal TransducingNeuronsCaspase 3Estrogen Receptor alphaTransfectionMolecular biologyRatsUp-RegulationDNA-Binding ProteinsProto-Oncogene Proteins c-bcl-2NeurologyCell cultureApoptosisCancer researchNeurology (clinical)Apoptosis Regulatory ProteinsEstrogen receptor alphahormones hormone substitutes and hormone antagonistsTranscription FactorsRestorative Neurology and Neuroscience
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Multiparametric evaluation of the cytoprotective effect of the Mangifera indica L. stem bark extract and mangiferin in HepG2 cells.

2012

Abstract Objective Mango (Mangifera indica L.) stem bark extract (MSBE) is a natural product with biological properties and mangiferin is the major component. This paper reported the evaluation of the protective effects of MSBE and mangiferin against the toxicity induced in HepG2 cells by tert-butyl hydroperoxide or amiodarone. Method Nuclear morphology, cell viability, intracellular calcium concentration and reactive oxygen species (ROS) production were measured by using a high-content screening multiparametric assay. Key findings MSBE and mangiferin produced no toxicity below 500 mg/ml doses. A marked recovery in cell viability, which was reduced by the toxicants, was observed in cells pr…

Cell SurvivalXanthonesPharmaceutical ScienceAmiodaronePharmacologychemistry.chemical_compoundtert-ButylhydroperoxidemedicineHumansMangiferaViability assayATP Binding Cassette Transporter Subfamily B Member 1MangiferinP-glycoproteinPharmacologychemistry.chemical_classificationReactive oxygen speciesMangiferabiologyDose-Response Relationship DrugPlant StemsPlant ExtractsHep G2 Cellsmedicine.diseaseCytoprotectionMitochondrial toxicityBiochemistrychemistryToxicitybiology.proteinPlant BarkCalciumReactive Oxygen SpeciesThe Journal of pharmacy and pharmacology
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The MDM2-p53 pathway is involved in preconditioning-induced neuronal tolerance to ischemia

2018

Brain preconditioning (PC) refers to a state of transient tolerance against a lethal insult that can be evoked by a prior mild event. It is thought that PC may induce different pathways responsible for neuroprotection, which may involve the attenuation of cell damage pathways, including the apoptotic cell death. In this context, p53 is a stress sensor that accumulates during brain ischemia leading to neuronal death. The murine double minute 2 gene (MDM2), a p53-specific E3 ubiquitin ligase, is the main cellular antagonist of p53, mediating its degradation by the proteasome. Here, we study the role of MDM2-p53 pathway on PC-induced neuroprotection both in cultured neurons (in vitro) and rat …

Cell death0301 basic medicineProgrammed cell deathCell SurvivalNeuronalScience2415 Biología MolecularIschemiaNeuroprotectionArticleBrain ischemiaMiceBrain ischemia03 medical and health sciences0302 clinical medicineIschemiaXarxes neuronals (Neurobiologia)medicineAnimalsIschemic PreconditioningCell damageCells CulturedBrain preconditioningNeuronsMultidisciplinarybiologyChemistryQRBrainProto-Oncogene Proteins c-mdm2MDM2-p53medicine.diseaseNeuroprotectionRatsCell biologyUbiquitin ligaseDisease Models Animal030104 developmental biology2490 Neurocienciasbiology.proteinMedicineIschemic preconditioningMdm2Tumor Suppressor Protein p53030217 neurology & neurosurgerySignal Transduction
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Oxidative stress resistance in hippocampal cells is associated with altered membrane fluidity and enhanced nonamyloidogenic cleavage of endogenous am…

2010

Reactive oxygen species (ROS) have important roles as signaling molecules in the regulation of a variety of biological processes. On the other hand, chronic oxidative stress exerted by ROS is widely considered a causative factor in aging. Therefore, cells need to be able to adapt to a chronic oxidative challenge and do so to a certain cell-type-specific extent. Recently, we have shown in oxidative-stress-resistant cell lines, HT22(H2O2) and HT22(Glu), derived from the neuronal cell line HT22 by chronic exposure to sublethal concentrations of H(2)O(2) and glutamate, that, in addition to the known antioxidant defense mechanisms, e.g., activation of antioxidant enzymes or up-regulation of heat…

Cell signalingMembrane FluidityBlotting WesternOxidative phosphorylationmedicine.disease_causeHippocampusBiochemistryNeuroprotectionCell LineAmyloid beta-Protein PrecursorMembrane MicrodomainsPhysiology (medical)Membrane fluidityAmyloid precursor proteinmedicineHumansCellular SenescenceNeuronschemistry.chemical_classificationReactive oxygen speciesbiologyChemistryCell MembraneMembrane ProteinsCell biologyOxidative Stressbiology.proteinSphingomyelinOxidative stressFree Radical Biology and Medicine
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New neuroprotective effect of lemon integropectin on neuronal cellular model

2021

Lemon IntegroPectin obtained via hydrodynamic cavitation of organic lemon processing waste in water shows significant neuroprotective activity in vitro, as first reported in this study investigating the effects of both lemon IntegroPectin and commercial citrus pectin on cell viability, cell morphology, reactive oxygen species (ROS) production, and mitochondria perturbation induced by treatment of neuronal SH-SY5Y human cells with H2O2. Mediated by ROS, including H2O2 and its derivatives, oxidative stress alters numerous cellular processes, such as mitochondrial regulation and cell signaling, propagating cellular injury that leads to incurable neurodegenerative diseases. These results, and t…

Cell signalingantioxidantPhysiologyhesperidin;Antioxidant Flavonoids Hesperidin Mitochondria Neu-roprotective Neurological disease Oxidative stress PectinClinical BiochemistryRM1-950antioxidant;MitochondrionCell morphologymedicine.disease_causeBiochemistryNeuroprotectionArticleflavonoids;03 medical and health sciences0302 clinical medicinehesperidinmedicineoxidative stressViability assayneurological diseaseMolecular Biology030304 developmental biologychemistry.chemical_classificationpectinoxidative stress;neuroprotective;0303 health sciencesReactive oxygen speciespectin;neuroprotectiveCell BiologyCell biologymitochondriachemistryneurological disease;flavonoidsTherapeutics. PharmacologyCellular model030217 neurology & neurosurgeryOxidative stress
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Brain and Cancer: The Protective Role of Erythropoietin

2005

Erythropoietin (Epo) is a pleiotropic agent, that is to say, it can act on several cell types in different ways. An independent system Epo/Epo receptor (EpoR) was detected in brain, leading to the hypothesis that this hormone could be involved in cerebral functions. Epo/EpoR expression changes during ontogenesis, thus indicating the importance of this system in neurodevelopment. Moreover, the hypoxia-induced production of Epo in the adult brain suggests that it could exert a neurotrophic and neuroprotective effect in case of brain injury. Epo could also influence neuro- transmission, inducing neurotransmitters (NT) release. Epo therapy in anemic cancer patients is still a controversial issu…

Cell typeCentral nervous systemPharmacologyModels BiologicalNeuroprotectionNeoplasmshemic and lymphatic diseasesDrug DiscoveryReceptors ErythropoietinmedicineAnimalsHumanscancerReceptorPleiotropyPharmacologyNeurotransmitter AgentsNeovascularization Pathologicbiologyhypoxiabusiness.industryMedicine (all)Organic ChemistryBrainangiogenesiGeneral MedicineNeuroprotectionneuroprotective effectErythropoietin receptorErythropoietin (Epo); brain; central nervous system (CNS) diseases; neuroprotective effectmedicine.anatomical_structureErythropoietin (Epo)Erythropoietinbiology.proteinMolecular MedicineerythropoietinSignal transductionbusinessNeurosciencecentral nervous system (CNS) diseasesmedicine.drugNeurotrophinChemInform
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