Search results for "Reactive"

showing 10 items of 1469 documents

Ursolic acid ameliorates stress and reactive oxygen species in C. elegans knockout mutants by the dopamine Dop1 and Dop3 receptors.

2020

Abstract Background Depression and stress-related disorders are leading causes of death worldwide. Standard treatments elevating serotonin or noradrenaline levels are not sufficiently effective and cause adverse side effects. A connection between dopamine pathways and stress-related disorders has been suggested. Compounds derived from herbal medicine could be a promising alternative. We examined the neuroprotective effects of ursolic acid (UA) by focusing on dopamine signalling. Methods Trolox equivalent capacity assay was used to determine the antioxidant activities of UA in vitro. C. elegans N2 wildtype and dopamine receptor-knockout mutants (dop-1-deficient RB665 and dop-3-deficient LX70…

Antioxidantmedicine.medical_treatmentDopamineLongevityPharmaceutical SciencePharmacologyNeuroprotectionAntioxidants03 medical and health scienceschemistry.chemical_compoundGene Knockout Techniques0302 clinical medicineDopamineStress PhysiologicalDrug DiscoverymedicineAnimalsHumansReceptorCaenorhabditis elegansCaenorhabditis elegans Proteins030304 developmental biologyPharmacologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesChemistryReceptors Dopamine D2Receptors Dopamine D1Receptors Dopamine D3TriterpenesMolecular Docking SimulationComplementary and alternative medicineDopamine receptor030220 oncology & carcinogenesisMutationMolecular MedicineSerotoninTroloxReactive Oxygen Speciesmedicine.drugSignal TransductionPhytomedicine : international journal of phytotherapy and phytopharmacology
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Melatonin protects against ischemia-reperfusion injury and inhibits apoptosis in isolated working rat heart.

2003

INTRODUCTION: Melatonin (MEL), a pineal hormone, is well known as a potent antioxidant in a variety of ischemia-reperfusion models. Recent studies have assumed a pivotal role of reactive oxygen species (ROS) in the development of apoptosis. There are few pieces of information concerning a possible protective role of MEL against apoptosis in ischemia-reperfusion injury of myocardium. METHODS: We conducted an in vitro experiment: (1) to study the effect of MEL in the model of isolated and perfused working rat heart; (2) to evaluate the antioxidant capacity of MEL by a simple fluorescence test; and (3) to analyze the extent of apoptosis inhibition by MEL. Four groups of male Wistar rat were us…

Antioxidantmedicine.medical_treatmentIschemiaPharmacologymedicine.disease_causePathology and Forensic MedicineMelatonin03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesPhysiology (medical)medicineneoplasms030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesTUNEL assaymedicine.disease3. Good healthchemistryApoptosisAnesthesiaReperfusion injury030217 neurology & neurosurgeryOxidative stressmedicine.drugPathophysiology : the official journal of the International Society for Pathophysiology
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The triterpenoid ursolic acid ameliorates stress in Caenorhabditis elegans by affecting the depression-associated genes skn-1 and prdx2.

2021

Abstract Introduction Depression is one of the leading causes of death worldwide. Lower antioxidant concentrations and increased oxidative stress levels contribute to the development of depression. Effective and tolerable medications are urgently needed. Nrf2 and PRDX2 are promising targets in the treatment of oxidative stress and, therefore, promising for the development of novel antidepressants. Ursolic acid (UA), a natural triterpenoid found in various plants is known to exert neuroprotective and antioxidant effects. Skn-1 (which corresponds to human Nrf2) and prdx2 deficient mutants of the nematode Caenorhabditis elegans are suitable models to study the effect of UA on these targets. Ad…

Antioxidantmedicine.medical_treatmentPharmaceutical SciencePharmacologymedicine.disease_causeProtective AgentsNeuroprotectionAntioxidants03 medical and health scienceschemistry.chemical_compound0302 clinical medicineUrsolic acidStress PhysiologicalDrug DiscoveryAdaptogenmedicineAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCaenorhabditis elegans030304 developmental biologyPharmacologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesbiologyDepressionPeroxiredoxinsbiology.organism_classificationAntidepressive AgentsTriterpenesDNA-Binding ProteinsMolecular Docking SimulationOxidative StressComplementary and alternative medicinechemistryGene Expression Regulation030220 oncology & carcinogenesisMutationMolecular MedicineReactive Oxygen SpeciesJugloneOxidative stressTranscription FactorsPhytomedicine : international journal of phytotherapy and phytopharmacology
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Proteomic Analysis of Saccharomyces cerevisiae Response to Oxidative Stress Mediated by Cocoa Polyphenols Extract

2020

The present study addressed the protective effects against oxidative stress (OS) of a cocoa powder extract (CPEX) on the protein expression profile of S. cerevisiae. A proteomic analysis was performed after culture preincubation with CPEX either without stress (&minus

Antioxidantmedicine.medical_treatmentSaccharomyces cerevisiaePharmaceutical Scienceantioxidant activitySaccharomyces cerevisiaeamino acid metabolismmedicine.disease_causeAmino acid metabolismAnalytical Chemistrycocoa polyphenolslcsh:QD241-441<i>Saccharomyces cerevisiae</i>03 medical and health sciencesHistone H3chemistry.chemical_compoundBiosynthesisAntioxidant activitylcsh:Organic chemistryprotein identificationDrug DiscoverymedicineDeletion mutantsoxidative stressPhysical and Theoretical ChemistryReactive oxygen species metabolic process030304 developmental biologychemistry.chemical_classification0303 health sciencesbiologyCocoa polyphenolsChemistry030302 biochemistry & molecular biologyOrganic Chemistrybiology.organism_classificationYeastAmino acidBiochemistryChemistry (miscellaneous)Oxidative stressMolecular MedicineProtein identificationdeletion mutantsOxidative stressMolecules
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Impact of Hydrogen Peroxide on Protein Synthesis in Yeast.

2021

This article belongs to the Special Issue Thiol-Based Redox Regulation of Cellular and Organismal Function.

Antioxidantprotein synthesisPhysiologymedicine.medical_treatmentClinical Biochemistryhydrogen peroxideReviewRM1-950Mitochondrionmedicine.disease_causeBiochemistryCysteine thiolscysteine thiolschemistry.chemical_compoundmedicineProtein biosynthesisHydrogen peroxideMolecular Biologychemistry.chemical_classificationReactive oxygen speciesTranslation (biology)Cell BiologyHydrogen peroxideSignalingCell biologychemistryTherapeutics. PharmacologyProtein synthesissignalingOxidative stressIntracellularAntioxidants (Basel, Switzerland)
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Cytoprotective effect of resveratrol diastereomers in CHO-K1 cells exposed to beauvericin

2015

Beauvericin (BEA) causes cytotoxicity, lipid peroxidation and reactive oxygen species in CHO-K1 cells. Resveratrol (RSV) is a polyphenol with multiple biological properties, including antioxidant effects. RSV has two forms: trans and cis. The aims of this study were to determine the cytoprotective effect of trans-RSV and diastereomers mixtures (50:50 trans/cis-RSV and 70:30 trans/cis-RSV) incubated alone and in combination with BEA in ovarian (CHO-K1) cells. The results demonstrated that cell viability increases (from 9% to 77%) when they were exposed to low concentration of RSV. Moreover, when the cells were pre-treated with RSV and then exposed to BEA, a cytoprotective effect (from 25% to…

Antioxidantvirusesmedicine.medical_treatmentCHO CellsResveratrolToxicologymedicine.disease_causeLipid peroxidationchemistry.chemical_compoundCricetulusCricetinaeDepsipeptidesStilbenesmedicineAnimalsViability assayCytotoxicitychemistry.chemical_classificationReactive oxygen speciesChemistryvirus diseasesGeneral Medicinerespiratory systemMolecular biologyBeauvericinBiochemistryCytoprotectionResveratrolLipid PeroxidationReactive Oxygen SpeciesOxidative stressFood ScienceFood and Chemical Toxicology
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Role of C-reactive protein in atherogenesis: can the apolipoprotein E knockout mouse provide the answer?

2005

Objective—Human C-reactive protein (CRP) was reported to accelerate atherosclerotic lesion development in male but not in female apolipoprotein E (apoE) knockout mice. Here, mice expressing rabbit CRP (rbCRP) were crossbred onto apoE knockout animals, and the effect on atherogenesis was studied.Methods and Results—Hemolytic complement activity could not be detected in apoE knockout mice. Furthermore, in contrast to human complement, neither rabbit nor human CRP complexed to modified low-density lipoprotein–activated murine complement. At 52 weeks, rbCRP levels were similar in male and female transgenic animals. Serum cholesterol levels were equivalent in female animals irrespective of rbCRP…

Apolipoprotein EMalemedicine.medical_specialtyPathologyRatónTransgeneHypercholesterolemiaMice TransgenicLesionMiceApolipoproteins ESpecies SpecificityInternal medicinemedicineAnimalsHumansTransgenesAortaMice KnockoutbiologyVascular diseaseC-reactive proteinCholesterol LDLComplement System Proteinsmedicine.diseaseAtherosclerosisComplement systemMice Inbred C57BLDisease Models AnimalEndocrinologyC-Reactive ProteinKnockout mousebiology.proteinFemaleDietary ProteinsRabbitsmedicine.symptomCardiology and Cardiovascular MedicineArteriosclerosis, thrombosis, and vascular biology
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Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

2007

Background— We have recently demonstrated that activity of red blood cell glutathione peroxidase-1 is inversely associated with the risk of cardiovascular events in patients with coronary artery disease. The present study analyzed the effect of glutathione peroxidase-1 deficiency on atherogenesis in the apolipoprotein E-deficient mouse. Methods and Results— Female apolipoprotein E-deficient mice with and without glutathione peroxidase-1 deficiency were placed on a Western-type diet for another 6, 12, or 24 weeks. After 24 weeks on Western-type diet, double-knockout mice (GPx-1 −/− ApoE −/− ) developed significantly more atherosclerosis than control apolipoprotein E-deficient mice. Moreover…

Apolipoprotein Emedicine.medical_specialtyGPX1AntioxidantApolipoprotein Bmedicine.medical_treatmentLipoproteinsApoptosisBlood Pressuremedicine.disease_causeNitric OxideMitochondria HeartMonocyteschemistry.chemical_compoundMiceApolipoproteins EGlutathione Peroxidase GPX1SuperoxidesInternal medicinePeroxynitrous AcidmedicineAnimalsAortaCell Proliferationchemistry.chemical_classificationMice KnockoutReactive oxygen speciesGlutathione PeroxidaseMembranesbiologyGlutathione peroxidaseGlutathioneAtherosclerosisEndocrinologyPhenotypechemistryImmunologybiology.proteinDisease ProgressionFemaleCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidation-ReductionOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Superoxide Flux in Endothelial Cells via the Chloride Channel-3 Mediates Intracellular Signaling

2007

Reactive oxygen species (ROS) have been implicated in both cell signaling and pathology. A major source of ROS in endothelial cells is NADPH oxidase, which generates superoxide (O2.−) on the extracellular side of the plasma membrane but can result in intracellular signaling. To study possible transmembrane flux of O2.−, pulmonary microvascular endothelial cells were preloaded with the O2.−-sensitive fluorophore hydroethidine (HE). Application of an extracellular bolus of O2.−resulted in rapid and concentration-dependent transient HE oxidation that was followed by a progressive and nonreversible increase in nuclear HE fluorescence. These fluorescence changes were inhibited by superoxide dism…

ApoptosisMembrane PotentialsSuperoxide dismutasechemistry.chemical_compoundChloride ChannelsSuperoxidesExtracellularAnimalsHumansEnzyme InhibitorsRNA Small InterferingMolecular BiologyLungCells CulturedFluorescent Dyeschemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideAngiotensin IIThrombinAcetophenonesEndothelial CellsNADPH OxidasesCell BiologyArticlesCell biologyMitochondriaPhenanthridinesOxygenchemistryDIDSbiology.proteinCalciumSignal transductionOxidation-ReductionIntracellularSignal Transduction
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Reactive oxygen species (ROS) generation inhibited by aporphine and phenanthrene alkaloids semi-synthesized from natural boldine.

2004

Four phenanthrene and one aporphine alkaloids semi-synthesized from boldine were evaluated for their inhibitory effect on reactive oxygen species (ROS) generation. ROS generation by neutrophils stimulated with N-formyl-methionyl-leucyl-phenylalanine was inhibited in a concentration dependent manner. Alkaloids exerted similar inhibitory effect in the hypoxanthine-xanthine oxidase system than in stimulated neutrophils, which could be attributed to a direct ROS scavenging activity. None of the alkaloids assayed had any effect on xanthine oxidase activity. Therefore the synthesized alkaloids might constitute an alternative therapy in inflammation disorders in which ROS generation is involved.

AporphinesStereochemistryNeutrophilsInflammationcomplex mixtureschemistry.chemical_compoundRos scavengingAlkaloidsDrug DiscoverymedicineBoldineHumansheterocyclic compoundsAporphineInhibitory effectchemistry.chemical_classificationReactive oxygen speciesOxidase testDose-Response Relationship DrugChemistryorganic chemicalsGeneral ChemistryGeneral MedicinePhenanthrenePhenanthrenesBiochemistrymedicine.symptomReactive Oxygen SpeciesChemicalpharmaceutical bulletin
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