Search results for "Hepatocyte"

showing 10 items of 369 documents

Chemical Composition, In Vitro Antitumor and Pro-Oxidant Activities of Glandora rosmarinifolia (Boraginaceae) Essential Oil

2018

The biological properties of essential oils have been demonstrated in the treatment of several diseases and to enhance the bioavailability of other drugs. In natural habitats the essential oils compounds may play important roles in the protection of the plants as antibacterials, antivirals, antifungals, insecticides and also against herbivores by reducing their appetite for such plants or by repelling undesirable others. We analyzed by gas-chromatography mass spectrometry the chemical composition of the essential oil of aerial parts of Glandora rosmarinifolia (Ten.) D.C. Thomas obtained by hydrodistillation and verified some biological activities on a panel of hepatocellular carcinoma cell …

0301 basic medicineChemical RadicalsAntioxidantmedicine.medical_treatmentMDA-MB-231Cancer Treatmentlcsh:MedicinenaphthoquinoneChemical CompositionBiochemistryPhysical ChemistryditerpeneAntioxidantslaw.invention0302 clinical medicinelawBreast TumorsSUM 149Medicine and Health SciencesBioassaySettore BIO/15 - Biologia FarmaceuticaCytotoxicitylcsh:ScienceMultidisciplinarybiologyTraditional medicineChemistryLiver DiseasesBoraginaceaeBoraginaceaeOxidantsHep3BLipidsChemistryOncology030220 oncology & carcinogenesisPhysical SciencesResearch ArticleHepG2Free RadicalsCell SurvivalGastroenterology and HepatologyCarcinomas03 medical and health sciencesInhibitory Concentration 50Cell Line TumorAromatic HydrocarbonsGastrointestinal TumorsBreast CancermedicineOils VolatileHumansPlant OilsEssential oilcytotoxic activityHA22T/VGH; HepG2; Hep3B; SUM 149; MDA-MB-231; cytotoxic activity; diterpenes; naphthoquinones; plant secondary metabolitesVolatile Organic CompoundsDose-Response Relationship DrugCell growthPlant ExtractsHA22T/VGHlcsh:RChemical CompoundsBiology and Life SciencesCancers and NeoplasmsEpithelial CellsHepatocellular CarcinomaSettore CHIM/06 - Chimica OrganicaPlant Components Aerialbiology.organism_classificationPro-oxidantplant secondary metabolitesAntineoplastic Agents PhytogenicHydrocarbonsBioavailability030104 developmental biologySettore BIO/03 - Botanica Ambientale E ApplicataHepatocytesSettore BIO/14 - Farmacologialcsh:QOils
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Drug metabolism by cultured human hepatocytes: how far are we from the in vivo reality?

2004

The investigation of metabolism is an important milestone in the course of drug development. Drug metabolism is a determinant of drug pharmacokinetics variability in human beings. Fundamental to this are phenotypic differences, as well as genotypic differences, in the expression of the enzymes involved in drug metabolism. Genotypic variability is easy to identify by means of polymerase chain reaction-based or DNA chip-based methods, whereas phenotypic variability requires direct measurement of enzyme activities in liver, or, indirectly, measurement of the rate of metabolism of a given compound in vivo. There is a great deal of phenotypic variability in human beings, only a minor part being…

0301 basic medicineDrugDiclofenacmedia_common.quotation_subjectBiologyPharmacologyToxicologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineCytochrome P-450 Enzyme SystemIn vivoGenetic variationmedicineHumansCells Culturedmedia_common030102 biochemistry & molecular biologyAnti-Inflammatory Agents Non-SteroidalGenetic VariationGeneral MedicineMetabolismIn vitroMedical Laboratory TechnologyDrug developmentBiochemistryLiverPharmaceutical Preparations030220 oncology & carcinogenesisMultigene FamilyHepatocytesAceclofenacDrug metabolismmedicine.drugAlternatives to laboratory animals : ATLA
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A Multi-Parametric Fluorescent Assay for the Screening and Mechanistic Study of Drug-Induced Steatosis in Liver Cells in Culture.

2017

Human hepatic cells have been used for drug safety risk evaluations throughout early development phases. They provide rapid, cost-effective early feedback to identify drug candidates with potential hepatotoxicity. This unit presents a cell-based assay to evaluate the risk of liver damage associated with steatogenic drugs. Detailed protocols for cell exposure to test compounds and for the assessment of steatosis-related cell parameters (intracellular lipid content, reactive oxygen species production, mitochondrial impairment, and cell death) are provided. A few representative results that illustrate the utility of this procedure for the screening of drug-induced steatosis are shown. © 2017 b…

0301 basic medicineDrugProgrammed cell deathmedia_common.quotation_subjectCellMitochondria LiverBiologyToxicology03 medical and health sciencesmedicineHumansCells Culturedmedia_commonchemistry.chemical_classificationReactive oxygen speciesCell Deathmedicine.diseaseLipid MetabolismFatty Liver030104 developmental biologymedicine.anatomical_structurechemistryBiochemistryLiverHigh-content screeningCancer researchHepatic stellate cellHepatocytesSteatosisChemical and Drug Induced Liver InjuryReactive Oxygen SpeciesIntracellularCurrent protocols in toxicologyLiterature Cited
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Upgrading HepG2 cells with adenoviral vectors that encode drug-metabolizing enzymes: application for drug hepatotoxicity testing.

2016

Drug attrition rates due to hepatotoxicity are an important safety issue considered in drug development. The HepG2 hepatoma cell line is currently being used for drug-induced hepatotoxicity evaluations, but its expression of drug-metabolizing enzymes is poor compared with hepatocytes. Different approaches have been proposed to upgrade HepG2 cells for more reliable drug-induced liver injury predictions. Areas covered: We describe the advantages and limitations of HepG2 cells transduced with adenoviral vectors that encode drug-metabolizing enzymes for safety risk assessments of bioactivable compounds. Adenoviral transduction facilitates efficient and controlled delivery of multiple drug-metab…

0301 basic medicineDrugmedia_common.quotation_subjectGenetic VectorsBiologyPharmacologyToxicologyENCODERisk AssessmentAdenoviridae03 medical and health sciencesToxicity TestsmedicineAnimalsHumansmedia_commonPharmacologyLiver injurychemistry.chemical_classificationReproducibility of ResultsGeneral MedicineHep G2 Cellsmedicine.disease030104 developmental biologyEnzymemedicine.anatomical_structureDrug developmentchemistryPharmaceutical PreparationsHepg2 cellsHepatocyteDrug DesignCancer researchHepatocytesChemical and Drug Induced Liver InjuryDrug metabolismExpert opinion on drug metabolismtoxicology
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Use of deep learning methods to translate drug-induced gene expression changes from rat to human primary hepatocytes

2020

In clinical trials, animal and cell line models are often used to evaluate the potential toxic effects of a novel compound or candidate drug before progressing to human trials. However, relating the results of animal and in vitro model exposures to relevant clinical outcomes in the human in vivo system still proves challenging, relying on often putative orthologs. In recent years, multiple studies have demonstrated that the repeated dose rodent bioassay, the current gold standard in the field, lacks sufficient sensitivity and specificity in predicting toxic effects of pharmaceuticals in humans. In this study, we evaluate the potential of deep learning techniques to translate the pattern of …

0301 basic medicineGene ExpressionGene Expression Regulation/drug effectsPathology and Laboratory MedicineConvolutional neural networkTOXICITYMachine LearningVoeding Metabolisme en GenomicaTime Measurement0302 clinical medicineGene expressionMedicine and Health SciencesMeasurementClinical Trials as TopicMultidisciplinaryArtificial neural networkPharmaceuticsQRMetabolism and GenomicsTOXICOGENOMICS030220 oncology & carcinogenesisMetabolisme en GenomicaMedicineEngineering and TechnologyNutrition Metabolism and GenomicsHepatocytes/drug effectsAlgorithmsResearch ArticleComputer and Information SciencesClinical Trials as Topic/statistics & numerical dataNeural NetworksGenetic ToxicologyTOXICOLOGYSciencePredictive ToxicologyComputational biologyBiologyComputer03 medical and health sciencesDose Prediction MethodsDeep LearningVoedingArtificial IntelligenceIn vivoGeneticsLife ScienceAnimalsHumansGeneNutritionbusiness.industryDeep learningBiology and Life SciencesGold standard (test)REPRESENTATIONSRats030104 developmental biologyGene Expression RegulationHepatocytesArtificial intelligenceNeural Networks ComputerToxicogenomicsbusinessNeuroscience
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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Efficacy of hydrodynamic interleukin 10 gene transfer in human liver segments with interest in transplantation.

2016

Different diseases lead, during their advanced stages, to chronic or acute liver failure, whose unique treatment consists in organ transplantation. The success of intervention is limited by host immune response and graft rejection. The use of immunosuppressant drugs generally improve organ transplantation, but they cannot completely solve the problem. Also, their management is delicate, especially during the early stages of treatment. Thus, new tools to set an efficient modulation of immune response are required. The local expression of interleukin (IL) 10 protein in transplanted livers mediated by hydrodynamic gene transfer could improve the organ acceptance by the host because it presents…

0301 basic medicineGraft Rejectionmedicine.medical_specialtyGenetic enhancementmedicine.medical_treatmentLiver transplantationOrgan transplantationEnd Stage Liver DiseaseTissue Culture Techniques03 medical and health sciencesImmune systemmedicineHumansTransplantation HomologousTransplantationHepatologybusiness.industryGraft SurvivalGene Transfer TechniquesInterleukinGenetic TherapyAllograftsInterleukin-10Liver TransplantationTransplantationInterleukin 10Microscopy Electron030104 developmental biologyLiverImmunologyCancer researchHepatocytesHydrodynamicsNanoparticlesSurgeryTransplantation ToleranceGoldbusinessEx vivoLiver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
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Rab33B Controls Hepatitis B Virus Assembly by Regulating Core Membrane Association and Nucleocapsid Processing

2017

Many viruses take advantage of cellular trafficking machineries to assemble and release new infectious particles. Using RNA interference (RNAi), we demonstrate that the Golgi/autophagosome-associated Rab33B is required for hepatitis B virus (HBV) propagation in hepatoma cell lines. While Rab33B is dispensable for the secretion of HBV subviral envelope particles, its knockdown reduced the virus yield to 20% and inhibited nucleocapsid (NC) formation and/or NC trafficking. The overexpression of a GDP-restricted Rab33B mutant phenocopied the effect of deficit Rab33B, indicating that Rab33B-specific effector proteins may be involved. Moreover, we found that HBV replication enhanced Rab33B expres…

0301 basic medicineHepatitis B virusBiologymedicine.disease_causeVirusArticleCell LineCell membraneRab33B03 medical and health sciencesnucleocapsid assemblyTranscription (biology)RNA interferenceVirologymedicineHumansSecretionNucleocapsidcore/capsid membrane associationHepatitis B virus030102 biochemistry & molecular biologyEffectorVirus AssemblyCell MembraneVirologyHepatitis B Core Antigenshepatitis B virus; Rab GTPase; Rab33B; core/capsid membrane association; nucleocapsid assembly; virus traffickingTransport proteinProtein Transport030104 developmental biologyInfectious Diseasesmedicine.anatomical_structurevirus traffickingrab GTP-Binding ProteinsHost-Pathogen InteractionsHepatocytesRab GTPaseViruses; Volume 9; Issue 6; Pages: 157
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Hepatitis B Virus Exploits ERGIC-53 in Conjunction with COPII to Exit Cells.

2020

Several decades after its discovery, the hepatitis B virus (HBV) still displays one of the most successful pathogens in human populations worldwide. The identification and characterization of interactions between cellular and pathogenic components are essential for the development of antiviral treatments. Due to its small-sized genome, HBV highly depends on cellular functions to produce and export progeny particles. Deploying biochemical-silencing methods and molecular interaction studies in HBV-expressing liver cells, we herein identified the cellular ERGIC-53, a high-mannose-specific lectin, and distinct components of the endoplasmic reticulum (ER) export machinery COPII as crucial factor…

0301 basic medicineHepatitis B virusSec24AEndosomeHBV assemblyVesicular Transport ProteinsN-glycosylationBiologymedicine.disease_causeEndoplasmic ReticulumTransfectionGenomeESCRTArticle03 medical and health sciencesN-linked glycosylationViral life cycleCell Line TumormedicineHBVHumansCOPIICOPIIlcsh:QH301-705.5Hepatitis B virus030102 biochemistry & molecular biologyEndosomal Sorting Complexes Required for TransportEndoplasmic reticulumVirionMembrane ProteinsGeneral MedicineHepatitis BHBV egressERGIC-53Cell biologyProtein Transport030104 developmental biologyMannose-Binding Lectinslcsh:Biology (General)HepatocytesLMAN-1COP-Coated VesiclesCells
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Functional inhibition of Oct leads to HNF4α upregulation

2021

Organic cation transporters (human, OCT; mouse, Oct) are responsible for the intracellular uptake and detoxification of a broad spectrum of endogenous and exogenous substrates. The OCT1 gene SLC22A1 (human; mouse, Scl22a1) is transactivated by hepatocyte nuclear factor 4α (human, HNF4α; mouse, Hnf4α). HNF4α is a master regulator of hepatocyte differentiation and is frequently associated with hepatocellular carcinoma (HCC). In addition, the downregulation of HNF4α is associated with enhanced fibrogenesis. Our recent study revealed that hepatocarcinogenesis and fibrosis were enhanced with the loss of Oct3 (gene, Slc22a3). Notably, differences in Hnf4α expression, and in cholestasis and fibros…

0301 basic medicineHepatocyte differentiationCancer ResearchOncogeneChemistryArticlesGeneral Medicineorganic cation transportermedicine.diseaseMolecular biology03 medical and health sciencesHepatocyte nuclear factors030104 developmental biology0302 clinical medicineImmunology and Microbiology (miscellaneous)CholestasisDownregulation and upregulationApoptosisFibrosis030220 oncology & carcinogenesisGene expressionmedicineSLC22A3HNF4αSLC22A1Experimental and Therapeutic Medicine
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