Search results for " preclinical"

showing 10 items of 159 documents

Nilotinib as Coadjuvant Treatment with Doxorubicin in Patients with Sarcomas: A Phase I Trial of the Spanish Group for Research on Sarcoma

2018

Abstract Purpose: Nilotinib plus doxorubicin showed to be synergistic regarding apoptosis in several sarcoma cell lines. A phase I/II trial was thus designed to explore the feasibility of nilotinib as coadjuvant of doxorubicin by inhibiting MRP-1/P-gp efflux activity. The phase I part of the study is presented here. Patients and Methods: Nilotinib 400 mg/12 hours was administered in fixed dose from day 1 to 6, and doxorubicin on day 5 of each cycle. Three dose escalation levels for doxorubicin at 60, 65, and 75 mg/m2 were planned. Cycles were repeated every 3 weeks for a total of 4 cycles. Eligible subtypes were retroperitoneal liposarcoma, leiomyosarcoma, and unresectable/metastatic high-g…

Male0301 basic medicineLeiomyosarcomaOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentDrug Evaluation PreclinicalApoptosisLiposarcomaNeutropeniaMice03 medical and health sciences0302 clinical medicineCell Line TumorInternal medicineAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineAnimalsHumansCell ProliferationNeoplasm StagingChemotherapybusiness.industrySarcomamedicine.diseasePyrimidines030104 developmental biologyOncologyNilotinibChemotherapy AdjuvantDoxorubicin030220 oncology & carcinogenesisFemaleSarcomaNeoplasm GradingChondrosarcomabusinessFebrile neutropeniamedicine.drugClinical Cancer Research
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Muricholic Acids Promote Resistance to Hypercholesterolemia in Cholesterol-Fed Mice

2021

International audience; Background and aims: Hypercholesterolemia is a major risk factor for atherosclerosis and cardiovascular diseases. Although resistant to hypercholesterolemia, the mouse is a prominent model in cardiovascular research. To assess the contribution of bile acids to this protective phenotype, we explored the impact of a 2-week-long dietary cholesterol overload on cholesterol and bile acid metabolism in mice. Methods: Bile acid, oxysterol, and cholesterol metabolism and transport were assessed by quantitative real-time PCR, western blotting, GC-MS/MS, or enzymatic assays in the liver, the gut, the kidney, as well as in the feces, the blood, and the urine. Results: Plasma tr…

Male0301 basic medicineMuricholic acidDrug Evaluation PreclinicalReceptors Cytoplasmic and NuclearCholesterol Dietarychemistry.chemical_compound0302 clinical medicineBiology (General)Spectroscopy2. Zero hungerKidney[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyBile acidChemistryGeneral Medicine3. Good healthComputer Science ApplicationsBlotChemistrymedicine.anatomical_structureCholesterolFXR030220 oncology & carcinogenesislipids (amino acids peptides and proteins)LXRmedicine.medical_specialtyOxysterolQH301-705.5medicine.drug_classHypercholesterolemiaArticleCatalysisBile Acids and SaltsInorganic Chemistry03 medical and health sciencesIn vivoInternal medicinemedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPhysical and Theoretical ChemistryLiver X receptorQD1-999Molecular BiologyCholesterolOrganic ChemistryCholic AcidsBile acidsMice Inbred C57BL030104 developmental biologyEndocrinology[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Both cholestatic and steatotic drugs trigger extensive alterations in the mRNA level of biliary transporters in rat hepatocytes: Application to devel…

2016

Disruption of the vectorial bile acid transport in the liver is a key feature of cholestatic drugs, although many causal and mechanistic aspects are still unknown. The aim of the present study was to explore if cholestatic drugs can repress or induce the expression of hepatic transporters. To this end, sandwich-cultured rat hepatocytes were treated with cholestatic and non-cholestatic (steatotic, non-hepatotoxic, etc.) drugs and the mRNA expression of 10 uptake and efflux biliary transporters was measured. Results evidenced that all cholestatic drugs cause extensive alterations in the mRNA expression of most biliary transporters. Surprisingly, nearly all steatotic drugs also affected the ex…

Male0301 basic medicinePathologymedicine.medical_specialtyDrug-Related Side Effects and Adverse ReactionsDrug Evaluation PreclinicalOrganic Anion Transporters Sodium-IndependentPharmacologyBiologyToxicology030226 pharmacology & pharmacyRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCholestasisPredictive Value of TestsIn vivomedicineAnimalsBileRNA MessengerCells CulturedCholestasisMultidrug resistance-associated protein 2Fatty liverTransporterGeneral Medicinemedicine.diseaseRatsFatty Liver030104 developmental biologyTetracyclinesHepatocytesBiomarker (medicine)EffluxSteatosisCarrier ProteinsBiomarkersToxicology Letters
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Glucagon-like peptide-2 treatment improves glucose dysmetabolism in mice fed a high fat diet

2016

Previous studies suggested that endogenous glucagon-like peptide 2 (GLP-2) is dispensable for the regulation of glucose homeostasis under normal conditions, while it can play a beneficial role in obesity conditions. The purpose of the present study was to investigate whether chronic treatment with Gly2-GLP-2, a stable analogue of GLP-2, can have an impact on glycaemic and lipid control in mice fed a high-fat diet (HFD), an animal model of human obesity and insulin resistance. HFD mice were treated once a day with Gly2-GLP-2 for 4 weeks. Body weight, food intake, fasting glucose, intraperitoneal glucose tolerance, insulin-induced glucose clearance, glucose-stimulated insulin secretion, β-cel…

Male0301 basic medicinemedicine.medical_specialtyEndocrinology Diabetes and MetabolismDrug Evaluation PreclinicalMicrovesicular SteatosisCarbohydrate metabolismDiet High-FatSettore BIO/09 - FisiologiaRandom Allocation03 medical and health sciencesEndocrinologyInsulin resistanceInternal medicineDiabetes mellitusGlucagon-Like Peptide 2medicineAnimalsGlucose homeostasisObesityPancreasPancreatic islets.Glucose Metabolism Disordersbusiness.industrydigestive oral and skin physiologyInsulin resistancemedicine.diseaseGlucagon-like peptide-2LipidsObesityMice Inbred C57BL030104 developmental biologyEndocrinologyLiverPeptidesbusinessGLP-2Dyslipidemia
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Treatment with soluble activin type IIB-receptor improves bone mass and strength in a mouse model of Duchenne muscular dystrophy.

2016

Background Inhibition of activin/myostatin pathway has emerged as a novel approach to increase muscle mass and bone strength. Duchenne muscular dystrophy (DMD) is a neuromuscular disorder that leads to progressive muscle degeneration and also high incidence of fractures. The aim of our study was to test whether inhibition of activin receptor IIB ligands with or without exercise could improve bone strength in the mdx mouse model for DMD. Methods Thirty-two mdx mice were divided to running and non-running groups and to receive either PBS control or soluble activin type IIB-receptor (ActRIIB-Fc) once weekly for 7 weeks. Results Treatment of mdx mice with ActRIIB-Fc resulted in significantly in…

MaleActivin Receptors Type IIDrug Evaluation PreclinicalOsteoclastsBone μCTBone and BonesMiceTGF-βsBone DensityPhysical Conditioning AnimalAnimalsBone ResorptionMuscle SkeletalExerciseOsteoblastsOrgan SizeMuscular Dystrophy AnimalCombined Modality TherapyBone-muscle interactionsAnimal modelsMice Inbred C57BLMuscular Dystrophy DuchenneDisease Models AnimalSolubilityMice Inbred mdxResearch ArticleBMC musculoskeletal disorders
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Analysis of early biochemical markers and regulation by tin protoporphyrin IX in a model of spontaneous osteoarthritis

2011

Abstract Age-related changes in joint tissues lead to osteoarthritis (OA). Detection of early changes in OA patients may help to initiate treatments before the establishment of irreversible joint destruction. STR/ort mice develop with age a severe degenerative joint disease that resembles human OA thus allowing the investigation of biochemical markers as well as new treatments in an accelerated time frame. We have analyzed the changes in serum levels of different mediators during the early phases of idiopathic OA in STR/ort mice. Serum levels of matrix metalloproteinase-3 (MMP-3) but not those of tumor necrosis factor-α, interleukin(IL)-1β, IL-17 or prostaglandin E 2 correlated with histopa…

MaleAgingmedicine.medical_specialtyPathologyMetalloporphyrinsmedicine.medical_treatmentDrug Evaluation PreclinicalProtoporphyrinsMice Inbred StrainsOsteoarthritisMatrix metalloproteinaseBiochemistryMiceEndocrinologyInternal medicineOsteoarthritisGeneticsmedicineAnimalsEnzyme InhibitorsMolecular BiologyBiochemical markersbusiness.industryInterleukinCell BiologyClinical Enzyme TestsTin protoporphyrin IXmedicine.diseaseArthritis ExperimentalEarly DiagnosisEndocrinologyHeme Oxygenase (Decyclizing)Disease ProgressionBiomarker (medicine)Matrix Metalloproteinase 3Tumor necrosis factor alphaInflammation MediatorsbusinessBiomarkersProstaglandin EExperimental Gerontology
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BCL-XL inhibition induces an FGFR4-mediated rescue response in colorectal cancer

2022

The heterogeneous therapy response observed in colorectal cancer is in part due to cancer stem cells (CSCs) that resist chemotherapeutic insults. The anti-apoptotic protein BCL-XL plays a critical role in protecting CSCs from cell death, where its inhibition with high doses of BH3 mimetics can induce apoptosis. Here, we screen a compound library for synergy with low-dose BCL-XL inhibitor A-1155463 to identify pathways that regulate sensitivity to BCL-XL inhibition and reveal that fibroblast growth factor receptor (FGFR)4 inhibition effectively sensitizes to A-1155463 both in vitro and in vivo. Mechanistically, we identify a rescue response that is activated upon BCL-XL inhibition and leads …

MaleBH3 mimeticsIndolesAxitinibColonDrug Evaluation Preclinicalbcl-X Proteincolorectal cancerMice SCIDGeneral Biochemistry Genetics and Molecular BiologyresistanceMice Inbred NODstem cellsCell Line TumorBCL-XLBCL-XL FGFR4 colorectal cancer apoptosis.AnimalsHumansReceptor Fibroblast Growth Factor Type 4BenzothiazolesAgedCell DeathDrug SynergismMiddle AgedIsoquinolinesOrganoidsNeoplastic Stem CellsFGFR4FemaleMCL-1Colorectal NeoplasmsCell reports
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Search for Stroke-Protecting Agents in Endothelin-1-Induced Ischemic Stroke Model in Rats

2012

Background and Objective. Ischemic stroke may initiate a reperfusion injury leading to brain damage cascades where inflammatory mechanisms play a major role. Therefore, the necessity for the novel stroke-protecting agents whose the mechanism of action is focused on their anti-inflammatory potency is still on the agenda for drug designers. Our previous studies demonstrated that cerebrocrast (a 1,4-dihydropyridine derivative) and mildronate (a representative of the aza-butyrobetaine class) possessed considerable anti-inflammatory and neuroprotective properties in different in vitro and in vivo model systems. The present study investigated their stroke-protecting ability in an endothelin-1 (ET…

MaleDihydropyridinesDrug Evaluation PreclinicalInfarctionBrain damagePharmacologyNeuroprotectionIn vivomedicineAnimalsRats WistarStrokeEndothelin-1business.industryGeneral Medicinemedicine.diseaseRatsStrokeDisease Models AnimalNeuroprotective AgentsMechanism of actionendothelin-1; ischemic stroke; neurodegeneration; protection; cerebrocrast; mildronateDrug Therapy Combinationmedicine.symptombusinessReperfusion injuryEx vivoMethylhydrazinesMedicina; Volume 48; Issue 10; Pages: 77
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Phospholipid breakdown and choline release under hypoxic conditions: inhibition by bilobalide, a constituent of Ginkgo biloba

1997

A marked increase of choline release from rat hippocampal slices was observed when the slices were superfused with oxygen-free buffer, indicating hypoxia-induced hydrolysis of choline-containing phospholipids. This increase of choline release was suppressed by bilobalide, an ingredient of Ginkgo biloba, but not by a mixture of ginkgolides. The EC50 value for bilobalide was 0.38 microM. In ex vivo experiments, bilobalide also inhibited hypoxia-induced choline release when given p.o. in doses of 2-20 mg/kg 1 h prior to slice preparation. The half-maximum effect was observed with 6 mg/kg bilobalide. A similar effect was noted after p.o. administration of 200 mg/kg EGb 761, a ginkgo extract con…

MaleDrug Evaluation PreclinicalCyclopentanesPharmacologyHippocampusCholinechemistry.chemical_compoundSlice preparationBilobalideAnimalsCholineRats WistarGinkgolidesFuransHypoxia BrainMolecular BiologyPhospholipidsEC50biologyPlant ExtractsGinkgo bilobaGeneral NeuroscienceGinkgobiology.organism_classificationRatsPlant LeavesGinkgolidesLogistic ModelschemistryBiochemistryNeurology (clinical)DiterpenesEx vivoDevelopmental BiologyBrain Research
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Endothelium- and nitric oxide-dependent vasorelaxing activities of gamma-butyrobetaine esters: possible link to the antiischemic activities of mildro…

2004

Mildronate [3-(2,2,2-trimethylhydrazine) propionate (THP)] is an antiischemic drug acting mainly via inhibition of fatty acid beta-oxidation. Some effects of the drug cannot be explained by the latter mechanism. We tested the eventual nitric oxide (NO) dependence of the mildronate action. Mildronate, gamma-butyrobetaine (GBB) and GBB methyl ester induced transient increases in nitric oxide (NO) concentrations in rat blood and myocardium. In vitro, these compounds neither modified the activities of purified neuronal and endothelial recombinant nitric oxide synthases (NOSs) nor were able to interact with their active site. GBB induced vasodilatation at high concentrations only (EC50 = 5 x 10(…

MaleEndotheliumNitric Oxide Synthase Type IIIStereochemistryDrug Evaluation PreclinicalMyocardial IschemiaVasodilationAorta ThoracicNitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundCarnitinemedicineAnimalsEndotheliumRats WistarPharmacologychemistry.chemical_classificationbiologyElectron Spin Resonance SpectroscopyActive siteFatty acidDrug SynergismRatsNitric oxide synthaseBetaineVasodilationDrug Combinationsmedicine.anatomical_structureEnzymeNG-Nitroarginine Methyl Esterchemistrybiology.proteinPropionateNitric Oxide SynthaseDitiocarbMethylhydrazinesEuropean journal of pharmacology
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