Search results for "SYNERGISM"

showing 10 items of 153 documents

The DNA methylation inhibitor 5-azacytidine modulates 6-thioguanine toxicity in mammalian cells

2003

In order to assess the effects of combining two antimetabolites used separately to treat human leukemias, we carried out an experimental study by exposing V79 Chinese hamster cells, a 6-thioguanine (6-tG)-sensitive cell line, to sequential and concurrent treatments with 5-azacytidine (5-azaC) and 6-tG. In this paper, we demonstrate that there is a clear dependency for the way in which this combination was tested. Pre-treatment with 5-azaC made V79 cells more resistant to 6-tG by a substantial reduction in 6-tG incorporation into DNA; this effect could still be detected for several cell divisions after the removal of 5-azaC, and was achieved neither by reduced cell growth nor by the inductio…

Antimetabolites AntineoplasticHypoxanthine Phosphoribosyltransferasemedicine.drug_classCell SurvivalCellHamsterToxicologyAntimetaboliteChinese hamster6-thioguanineCricetulus5-azacytidineCricetinaeAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsThioguanineCells CulturedbiologyCell growthtoxicityDrug SynergismGeneral MedicineDNAProdrugDNA Methylationbiology.organism_classificationMolecular biologySettore BIO/18 - Geneticamedicine.anatomical_structureBiochemistryCell cultureToxicityAzacitidineSister Chromatid ExchangeCell Division
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Effects of soyasaponin I and soyasaponins-rich extract on the Alternariol-induced cytotoxicity on Caco-2 cells

2015

Abstract Alternariol (AOH) is a mycotoxin produced by Alternaria spp. Soyasaponin I (Ss-I) is present naturally in legumes, and it has antioxidant properties. Cytotoxic and genotoxic effects of AOH have been demonstrated previously in vitro. In the present study, the cytotoxicity of AOH, Ss-I, and soyasaponins-rich extract from lentils was investigated; as well as, the cytoprotective effects of Ss-I and lentil extracts against AOH induced-cytotoxicity on Caco-2 cells. Cytotoxicity was carried out using MTT and PC assays (AOH: 3.125–100 µM, Ss-I: 3.125–50 µM, and lentil extracts: 1:0–1:32) during 24 h of exposure. Only AOH showed cytotoxic effect. The reduction in cell proliferation ranged f…

AntioxidantCell SurvivalStereochemistrymedicine.medical_treatmentAlternariolBiologyToxicologyAntioxidantsLactoneschemistry.chemical_compoundmedicineHumansCytotoxic T cellFood scienceOleanolic AcidCytotoxicityMycotoxinCell ProliferationPlant ExtractsCell growthAlternariaDrug SynergismGeneral MedicineMycotoxinsSaponinsIn vitrochemistryCytoprotectionCaco-2Lens PlantCaco-2 CellsDNA DamageFood ScienceFood and Chemical Toxicology
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Betacyanins as phenol antioxidants. Chemistry and mechanistic aspects of the lipoperoxyl radical-scavenging activity in solution and liposomes.

2009

Reaction kinetics of betanin and its aglycone betanidin towards peroxyl radicals generated from the azo-initiated oxidation of methyl linoleate in methanol, and of a heterogeneous aqueous/soybean phosphatidylcholine liposomal system, were studied by monitoring formation of linoleic acid hydroperoxides and consumption of the pigments. Betanin was a weak retarder in methanol, and an effective chain breaking antioxidant in the liposomal model, indicating that kinetic solvent effects and partition in lipid bilayers may affect its activity. Betanidin behaved as a chain terminating antioxidant in both models. Kinetic parameters characterizing peroxyl radical-scavenging activity showed that betani…

Antioxidantmedicine.medical_treatmentLipid Bilayersalpha-TocopherolBiochemistryChemical kineticsLinoleic Acidchemistry.chemical_compoundStructure-Activity RelationshipReaction rate constantSettore BIO/10 - BiochimicamedicineBetacyaninsOrganic chemistryChromatography High Pressure LiquidBetaninAqueous solutionMolecular StructureMethanolWaterDrug SynergismGeneral MedicineFree Radical ScavengersSolutionsAglyconechemistryLinoleic Acidsbetacyanins betanin betanidin lipid peroxides liposomes antioxidant phytochemicalsSpectrophotometryLiposomesPhosphatidylcholinesSolventsMethanolBetacyaninsLipid PeroxidationOxidation-ReductionFree radical research
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Heme oxygenase-1 induction by nitric oxide in RAW 264.7 macrophages is upregulated by a cyclo-oxygenase-2 inhibitor.

2001

Unstimulated RAW 264.7 macrophages express negligible heme oxygenase-1 (HO-1) protein but incubation with the nitric oxide (NO) donor spermine nonoate (SPNO) induced HO-1 and weakly cyclo-oxygenase-2 (COX-2) protein. This effect was potentiated by coincubation with the COX-2 selective inhibitor, SC58125. Cells incubated with SPNO showed a strong increase in HO-1 mRNA levels after 4 h with a significant potentiation in the presence of SC58125, which did not modify HO-1 mRNA stability. The induction of HO-1 by NO and its potentiation by anti-inflammatory agents may play a role in inflammatory and immune responses.

BiophysicsSpermineNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundMiceDownregulation and upregulationMacrophageAnimalsCyclooxygenase InhibitorsRNA MessengerMolecular BiologyHemeCyclooxygenase 2 InhibitorsMacrophagesMembrane ProteinsLong-term potentiationDrug SynergismMolecular biologyUp-RegulationHeme oxygenaseIsoenzymeschemistryBiochemistryCell cultureCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesHeme Oxygenase (Decyclizing)PyrazolesNitrogen OxidesSpermineHeme Oxygenase-1Biochimica et biophysica acta
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Synergistic interaction of adenylate cyclase activators and nitric oxide donor SIN-1 on platelet cyclic AMP

1995

Abstract The molecular mechanism of the synergistic platelet inhibition by activators of adenylate cyclase and guanylate cyclase in human platelets was investigated. The adenylate cyclase activators iloprost and prostaglandin E 1 and the guanylate cyclase activator 3-morpholino-synonimine (SIN-1) dose-dependently inhibited thrombin-induced aggregation of washed human platelets. Furthermore, SIN-1 at a concentration inhibiting platelet aggregation by only 10% shifted the IC 50 values of iloprost and prostaglandin E 1 by one order of magnitude to the left, indicating a synergistic action of adenylate cyclase and guanylate cyclase activators. Iloprost and prostaglandin E 1 dose-dependently ele…

Blood Plateletsmedicine.medical_specialtyGUCY1B3Platelet Aggregationmedicine.medical_treatmentAdenylate kinaseIn Vitro TechniquesNitric OxideCyclasechemistry.chemical_compoundInternal medicineCyclic AMPmedicineHumansPlateletIloprostAlprostadilCyclic GMPPharmacologyForskolinGUCY1A3PhosphodiesteraseDrug SynergismEnzyme ActivationEndocrinologychemistryGuanylate CyclaseMolsidominelipids (amino acids peptides and proteins)Platelet Aggregation InhibitorsAdenylyl CyclasesProstaglandin EEuropean Journal of Pharmacology: Molecular Pharmacology
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Budesonide/formoterol for the treatment of asthma.

2003

Budesonide/formoterol (Symbicort), AstraZeneca plc) is a novel treatment for asthma, combining an inhaled corticosteroid - budesonide, and a long-acting beta(2)-agonist - formoterol, in a single inhaler, the Turbuhaler. Randomised, clinical studies in patients with asthma have demonstrated that budesonide/formoterol is more effective than the inhaled corticosteroids, budesonide and fluticasone alone, and at least as effective as both monocomponents in separate inhalers. Results from clinical studies suggest a synergistic effect when both drugs are administered via one inhaler, although the mechanisms for this are not fully understood. Budesonide/formoterol has a rapid onset of effect, appar…

Budesonideimmune system diseasesFormoterol FumaratemedicineHumansPharmacology (medical)Anti-Asthmatic AgentsBudesonideChildAsthmaFluticasonePharmacologyCOPDbusiness.industryInhalerDrug SynergismGeneral Medicinerespiratory systemmedicine.diseaseAsthmarespiratory tract diseasesDrug CombinationsBudesonide/formoterolEthanolaminesAnesthesiaFormoterol FumarateFormoterolbusinesshormones hormone substitutes and hormone antagonistscirculatory and respiratory physiologymedicine.drugExpert opinion on pharmacotherapy
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Rate-retarding effects of mixed anionic/non-ionic micelles on the alkaline hydrolysis of the chloropentamminocobalt(III) complex - Role of the anioni…

2006

Rate data for the alkaline hydrolysis of the chloropentaamminecobalt(III) cation in the presence of mixed micelles composed of (i) anionic sodium decylsulphate (SDeS) and non-ionic dodecylpenta(oxyethylene glycol) monoether (C12E5) surfactants and (ii) anionic sodium perfluorooctanoate (SPFO) and non-ionic C12E5 surfactants has been obtained at T 298K and constant electrolyte concentration 0.08 mol dm−3 ([NaOH] = 0.01 mol dm−3, [NaClO4] = 0.07 mol dm−3) over a wide range of total surfactant concentration (Ct) and anionic mole fraction (χ). The critical micelle concentrations (c.m.c.s) of the mixed micelles have been determined over the entire χ range by means of surface tension measurements…

CHLOROPENTAAMMINECOBALT(III) CATIONSYSTEMSSODIUM DODECYL-SULFATEBASE HYDROLYSISMICELLIZATIONBINARY-MIXTURESSYNERGISM
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The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism

2012

In a previous work of ours dehydroxymethyl-epoxyquinomicin (DHMEQ), an inhibitor of NF-κB, was shown to induce apoptosis through Reactive Oxygen Species (ROS) production in hepatoma cells. The present study demonstrated that DHMEQ cooperates with Celecoxib (CLX) to decrease NF-κB DNA binding and to inhibit cell growth and proliferation more effectively than treatment with these single agents alone in the hepatoma cell lines HA22T/VGH and Huh-6. ROS production induced by the DHMEQ-CLX combination in turn generated the expression of genes involved in endoplasmic reticulum (ER) stress and silencing TRB3 mRNA significantly decreased DHMEQ-CLX-induced cell growth inhibition. Moreover, the DHMEQ-…

Cancer ResearchCarcinoma HepatocellularAntineoplastic AgentsApoptosisCell Cycle ProteinsProtein Serine-Threonine KinasesBiologyDHMEQ Celecoxib NF-jB CD95/CD95L Liver cancer cellsCell Line TumorSurvivinHumansGene silencingfas ReceptorProtein kinase BCell ProliferationSulfonamidesGene knockdownCyclooxygenase 2 InhibitorsCyclohexanonesCell growthEndoplasmic reticulumLiver NeoplasmsNF-kappa BDrug SynergismEndoplasmic Reticulum StressMolecular biologyAcetylcysteineRepressor ProteinsOncologyCelecoxibCell cultureApoptosisBenzamidesCancer researchPyrazolesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesCancer Letters
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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Effects of resveratrol analogs on cell cycle progression, cell cycle associated proteins and 5fluoro-uracil sensitivity in human derived colon cancer…

2009

International audience; Epidemiological studies suggested that trans-resveratrol, a wine grape component, could prevent malignant tumor development. This compound also demonstrated cytostatic and cytotoxic effects on tumor cells in vitro. To obtain trans-resveratrol derivatives with a better cellular uptake and enhanced antiproliferative effects, we synthesized a triacetate derivative as well as an oligomer, epsilon-viniferin and its acetylated form, epsilon-viniferin penta-acetate. We also obtained vineatrol, a wine grape shoot extract that associates several polyphenols that may act synergistically, including trans-resveratrol and epsilon-viniferin. We show here that resveratrol triacetat…

Cancer ResearchCyclin AFluorescent Antibody TechniqueCell Cycle ProteinsMESH: Cell CycleMESH: Flow CytometryMESH : Blotting WesternResveratrolmedicine.disease_causeWine grapeMESH: Drug SynergismImmunoenzyme Techniqueschemistry.chemical_compoundMESH: PhenolsMESH : Cell Cycle ProteinsMESH : Tumor Cells CulturedMESH: StilbenesStilbenesTumor Cells CulturedMESH : Cell ProliferationMESH: Fluorescent Antibody TechniqueMESH: Antimetabolites AntineoplasticbiologyKinaseMESH : Antimetabolites AntineoplasticCell Cyclefood and beveragesDrug SynergismCell cycleFlow CytometryMESH : Colonic NeoplasmsOncologyBiochemistryColonic NeoplasmsMESH : FluorouracilFluorouracilMESH : PhenolsAntimetabolites AntineoplasticMESH : Drug SynergismMESH : Flow CytometryBlotting WesternMESH : ImmunoprecipitationMESH : StilbenesMESH: Cell Cycle ProteinsPhenolsMESH : Immunoenzyme TechniquesMESH: Cell ProliferationMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansImmunoprecipitationMESH: Blotting Western[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Tumor Cells CulturedKinase activityMESH: Immunoenzyme Techniques[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBenzofuransCell ProliferationMESH: Colonic NeoplasmsMESH: HumansMESH : BenzofuransMESH: ImmunoprecipitationMESH : HumansMESH: BenzofuransMESH : Fluorescent Antibody TechniquechemistryResveratrolCell culturebiology.proteinCarcinogenesisMESH: Fluorouracil
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