Search results for "Oxazines"

showing 10 items of 108 documents

Evidence for a modulatory role of cannabinoids on the excitatory NANC neurotransmission in mouse colon

2007

Abstract It is well accepted that endogenous cannabinoids and CB1 receptors are involved in the regulation of smooth muscle contractility and intestinal motility, through a mechanism mainly related to reduction of acetylcholine release from cholinergic nerve endings. Because, few data exist on a possible modulatory action of the cannabinoid agents on the non-adrenergic non-cholinergic (NANC) excitatory and inhibitory neurotransmission, the aim of the present study was to investigate the effects of cannabinoid drugs on the NANC responses elicited by electrical field stimulation (EFS) in the circular muscle of mouse proximal colon. Colonic contractions were monitored as changes in endoluminal…

CB1 receptorIndolesCannabinoid receptormedicine.medical_treatmentSynaptic TransmissionSettore BIO/09 - FisiologiaEnteric Nervous SystemReceptor Cannabinoid CB2Micechemistry.chemical_compoundPiperidinesReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid receptor type 2musculoskeletal neural and ocular physiologyAnandamideSmooth muscle contractionRimonabantAgonistmedicine.medical_specialtyColonPolyunsaturated Alkamidesmedicine.drug_classMorpholinesNeuromuscular JunctionArachidonic AcidsIn Vitro TechniquesNaphthalenesTachykininsInternal medicineCannabinoid Receptor ModulatorsIntestinal motilitymedicineAnimalsCannabinoidReceptors TachykininPharmacologyDose-Response Relationship DrugCannabinoidsExcitatory Postsynaptic PotentialsNANC relaxationURB597Electric StimulationBenzoxazinesMice Inbred C57BLEndocrinologyInhibitory Postsynaptic PotentialschemistryPyrazolesNANC contractionCannabinoidGastrointestinal MotilityEndocannabinoidsPharmacological Research
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Selectivity analysis of protein kinase CK2 inhibitors DMAT, TBB and resorufin in cisplatin-induced stress responses.

2009

Udgivelsesdato: 2009-Nov Targeting protein kinases as a therapeutic approach to treat various diseases, especially cancer is currently a fast growing business. Although many inhibitors are available, exhibiting remarkable potency, the major challenge is their selectivity. Here we show that the protein kinase CK2 inhibitors DMAT, TBB and resorufin differ in their selectivity against PI3K family members, since PI3K and DNA-PK are subject to inhibition by DMAT and TBB, however, not by resorufin. TBB and DMAT treatment together with cisplatin lead to an inhibition of cisplatin-induced stress signaling (as detected by phosphorylation of JNK and H2AX). In the case of resorufin no interference wit…

Cancer ResearchKinaseCell SurvivalBlotting WesternAntineoplastic AgentsCell cycleBiologyTriazolesCell killingOncologyBiochemistryApoptosisStress PhysiologicalCell Line TumorOxazinesPhosphorylationHumansBenzimidazolesViability assayCasein kinase 2Signal transductionCisplatinEnzyme InhibitorsCasein Kinase IISignal TransductionInternational journal of oncology
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WIN induces apoptotic cell death in human colon cancer cells through a block of autophagic flux dependent on PPARγ down-regulation.

2014

Cannabinoids have been reported to possess anti-tumorigenic activity in cancer models although their mechanism of action is not well understood. Here, we show that the synthetic cannabinoid WIN55,212-2 (WIN)-induced apoptosis in colon cancer cell lines is accompanied by endoplasmic reticulum stress induction. The formation of acidic vacuoles and the increase in LC3-II protein indicated the involvement of autophagic process which seemed to play a pro-survival role against the cytotoxic effects of the drug. However, the enhanced lysosomal membrane permeabilization (LMP) blocked the autophagic flux after the formation of autophagosomes as demonstrated by the accumulation of p62 and LC3, two ma…

Cancer ResearchMorpholinesClinical BiochemistryPharmaceutical ScienceDown-RegulationAntineoplastic AgentsApoptosisBiologyNaphthalenesDownregulation and upregulationSettore BIO/10 - BiochimicaCell Line TumormedicineAutophagyGene silencingHumansViability assayPharmacologyEndoplasmic reticulumBiochemistry (medical)AutophagyCannabinoids PPARγ ER stress autophagy/apoptosis interplay colon carcinoma cellsCell BiologyEndoplasmic Reticulum StressCell biologyBenzoxazinesMitochondriaPPAR gammaMechanism of actionApoptosisColonic NeoplasmsUnfolded protein responsemedicine.symptomSignal TransductionApoptosis : an international journal on programmed cell death
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Apoptosis induced in HepG2 cells by the synthetic cannabinoid WIN: involvement of the transcription factor PPARgamma.

2008

It has recently been shown that cannabinoids induce growth inhibition and apoptosis in different tumour cell lines. In the current study, the effects of WIN 55,212-2 (WIN), a synthetic and potent cannabinoid receptor agonist, are investigated in hepatoma HepG2 cells and a possible signal transduction pathway is proposed. In these cells, WIN induces a clear apoptotic effect which was accompanied by up-regulation of the death-signalling factors Bax, Bcl-X(S), t-Bid and down-regulation of the survival factors survivin, phospho-AKT, Hsp72 and Bcl-2. Moreover, WIN-induced apoptosis is associated with JNK/p38 MAPK pathway activation and mitochondrial depolarisation demonstrated by a cytofluorimet…

Cannabinoid receptorCarcinoma HepatocellularCell SurvivalPyridinesmedicine.medical_treatmentp38 mitogen-activated protein kinasesMorpholinesApoptosisBiologyNaphthalenesBiochemistryReceptor Cannabinoid CB2Membrane Microdomainscannabinoids PPARgamma factor apoptosis cancer cellsSettore BIO/10 - BiochimicaCell Line TumorSurvivinmedicineHumansAnilidesViability assayCannabinoidsLiver NeoplasmsGeneral MedicineCell biologyBenzoxazinesPPAR gammaApoptosisCancer cellBenzamidesCannabinoidSignal transductionApoptosis Regulatory ProteinsProtein KinasesSignal TransductionBiochimie
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The Endocannabinoid System Promotes Astroglial Differentiation by Acting on Neural Progenitor Cells

2006

Endocannabinoids exert an important neuromodulatory role via presynaptic cannabinoid CB1receptors and may also participate in the control of neural cell death and survival. The function of the endocannabinoid system has been extensively studied in differentiated neurons, but its potential role in neural progenitor cells remains to be elucidated. Here we show that the CB1receptor and the endocannabinoid-inactivating enzyme fatty acid amide hydrolase are expressed, bothin vitroandin vivo, in postnatal radial glia (RC2+cells) and in adult nestin type I (nestin+GFAP+) neural progenitor cells. Cell culture experiments show that CB1receptor activation increases progenitor proliferation and differ…

Cannabinoid receptorCellular differentiationMorpholinesApoptosisNerve Tissue ProteinsBiologyNaphthalenesHippocampusAmidohydrolasesNestinMiceIntermediate Filament ProteinsReceptor Cannabinoid CB1Cannabinoid Receptor ModulatorsGlial Fibrillary Acidic ProteinAnimalsProgenitor cellEnzyme InhibitorsNeural cellCells CulturedProgenitorMice KnockoutNeuronsCannabinoidsmusculoskeletal neural and ocular physiologyGeneral NeuroscienceStem CellsCell DifferentiationArticlesNestinEndocannabinoid systemNeural stem cellBenzoxazinesRatsnervous systemAstrocytesBenzamideslipids (amino acids peptides and proteins)CarbamatesNeurosciencepsychological phenomena and processesEndocannabinoids
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WIN55,212-2-induced expression of Mir-29b1 favours the suppression of osteosarcoma cell migration in a SPARC-independent manner

2019

WIN55,212-2 (WIN) is a synthetic agonist of cannabinoid receptors that displays promising antitumour properties. The aim of this study is to demonstrate that WIN is able to block the migratory ability of osteosarcoma cells and characterize the mechanisms involved. Using wound healing assay and zymography, we showed that WIN affects cell migration and reduces the activity of the metalloproteases MMP2 and MMP9. This effect seemed to be independent of secreted protein acidic and rich in cysteine (SPARC), a matricellular protein involved in tissue remodeling and extracellular matrix deposition. SPARC release was indeed prevented by WIN, and SPARC silencing by RNA interference did not influence …

Cannabinoid receptorMorpholinesAntineoplastic AgentsMMP9NaphthalenesCatalysisArticlelcsh:ChemistryInorganic ChemistryExtracellular matrixExtracellular VesiclescannabinoidsDownregulation and upregulationCell MovementCell Line TumorSettore BIO/10 - BiochimicaGene silencingHumansOsteonectinCell migrationPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyCannabinoidSpectroscopyCell ProliferationOsteosarcomaChemistryCell growthOrganic ChemistryMatricellular proteinCell migrationSPARCGeneral MedicineComputer Science ApplicationsCell biologyBenzoxazinesMiR-29b1MicroRNAslcsh:Biology (General)lcsh:QD1-999
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Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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The Synthetic Cannabinoid WIN 55,212-2 Sensitizes Hepatocellular Carcinoma Cells to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-I…

2010

In this article, we demonstrate that the synthetic cannabinoid R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicat…

Carcinoma HepatocellularDNA ComplementaryMorpholinesApoptosisNaphthalenesCHOPMembrane PotentialsTNF-Related Apoptosis-Inducing LigandCell Line TumorSurvivinmedicineHumansWIN 55212-2Protein kinase BTranscription factorCaspaseDNA PrimersPharmacologybiologyCannabinoidsReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsGene AmplificationDNA NeoplasmFlow CytometryBenzoxazinesReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMitochondrial MembranesImmunologybiology.proteinCancer researchMolecular MedicineTumor necrosis factor alphaTranscription Factor CHOPmedicine.drugMolecular Pharmacology
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Cytotoxicity of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide in multidrug-resistant cancer cells through activation of PERK/eIF2α/AT…

2021

After decades of research, multidrug resistance (MDR) remains a huge challenge in cancer treatment. In this study, the cytotoxic of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide (MCC1734) has been investigated towards multidrug-resistant cancer cell lines. MCC1734 exerted cytotoxicity on cell lines expressing different mechanisms of drug resistance (P-glycoprotein, BCRP, ABCB5, EGFR, p53 knockout) to a different extent. Interestingly, sensitive CCRF-CEM cells and multidrug-resistant P-gp-overexpressing CEM/ADR5000 cells represented similar sensitivity towards MCC1734, indicating MCC1734 can bypass P-gp-mediated resistance. Microarray-based mRNA expression revealed that MCC17…

Cell SurvivalEukaryotic Initiation Factor-2Antineoplastic AgentsMitochondrionBiochemistryFlow cytometryeIF-2 KinaseCell Line TumorOxazinesmedicineHumansCytotoxic T cellGene Regulatory NetworksCytotoxicityPharmacologyMolecular Structuremedicine.diagnostic_testChemistryCell cycleActivating Transcription Factor 4Gene Expression Regulation NeoplasticXanthenesDrug Resistance NeoplasmCell cultureApoptosisCancer cellCancer researchGene DeletionBiochemical Pharmacology
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