Search results for "Caspase"

showing 10 items of 390 documents

Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothal…

2015

Endocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamine…

AstrocitosNeurobiologia del desenvolupamentAmidohidrolasasCannabinoid receptorCarbamatos:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Intracellular Signaling Peptides and Proteins::Apoptosis Regulatory Proteins::Caspases [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Differentiation::Neurogenesis [Medical Subject Headings]medicine.medical_treatment:Chemicals and Drugs::Carbohydrates::Monosaccharides::Hexoses::Glucose [Medical Subject Headings]Apoptosis:Phenomena and Processes::Physiological Phenomena::Body Constitution::Body Weights and Measures::Body Size::Body Weight [Medical Subject Headings]chemistry.chemical_compound:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Membrane Proteins::Receptors Cell Surface::Receptors G-Protein-Coupled::Receptors Cannabinoid::Receptor Cannabinoid CB1 [Medical Subject Headings]0302 clinical medicine:Chemicals and Drugs::Organic Chemicals::Carboxylic Acids::Acids Acyclic::Carbamates [Medical Subject Headings]Fatty acid amide hydrolaseReceptor cannabinoide CB1:Organisms::Eukaryota::Animals [Medical Subject Headings]FAAHGliosishealth care economics and organizations:Chemicals and Drugs::Nucleic Acids Nucleotides and Nucleosides::Nucleosides::Deoxyribonucleosides::Deoxyuridine::Bromodeoxyuridine [Medical Subject Headings]:Chemicals and Drugs::Lipids::Glycerides::Triglycerides [Medical Subject Headings]Original Research0303 health sciencesNeurogenesisBenzamidas:Chemicals and Drugs::Polycyclic Compounds::Steroids::Cholestanes::Cholestenes::Cholesterol [Medical Subject Headings]Endocannabinoid systemEtanolaminas3. Good healthEndocannabinoides:Chemicals and Drugs::Lipids::Fatty Acids::Fatty Acids Unsaturated::Fatty Acids Monounsaturated::Oleic Acids [Medical Subject Headings]CannabinoidesMicroglíalipids (amino acids peptides and proteins)medicine.symptomColesterol:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Terpenes::Cannabinoids [Medical Subject Headings]:Chemicals and Drugs::Lipids::Fatty Acids::Palmitic Acids [Medical Subject Headings]psychological phenomena and processesProliferación celularmedicine.medical_specialtyCerebroNeurogenesiseducationBiologyBromodesoxiuridina:Anatomy::Nervous System::Neuroglia::Microglia [Medical Subject Headings]Triglicéridoslcsh:RC321-571Ácidos oléicosRatas03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineHipocampomedicineCaspasa 3:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hippocampus [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry030304 developmental biologyPalmitoylethanolamide:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Neurotransmitter Agents::Endocannabinoids [Medical Subject Headings]:Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Amidohydrolases [Medical Subject Headings]Cannabinoids:Anatomy::Cells::Neuroglia::Astrocytes [Medical Subject Headings]Peso corporalEnergy metabolism:Anatomy::Nervous System::Central Nervous System::Brain [Medical Subject Headings]:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hypothalamus [Medical Subject Headings]URB597:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death [Medical Subject Headings]:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Gliosis [Medical Subject Headings]:Chemicals and Drugs::Organic Chemicals::Amines::Amino Alcohols::Ethanolamines [Medical Subject Headings]Muerte celular:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings]EndocrinologyURB597chemistryGliosisnervous systemGlucosaCannabinoidEnergy Metabolism:Chemicals and Drugs::Organic Chemicals::Amides::Benzamides [Medical Subject Headings]HipotálamoÁcidos palmíticos030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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Caractérisation des figures myéliniques associées à l'accumulation de lipides polaires induites par différents oxystérols cytotoxiques identifiés dan…

2006

Atherosclerosis is a complex and chronic arterial process which is characterized by a remodeling of the vascular wall, associated with inflammatory reactions, proliferation and cell death process, and with accumulation of oxidized lipids among which oxysterols (cholesterol oxidation products) which might play key roles in the initiation and development of atheromatous lesions. Our work performed on U937 and THP1 promonocytic cells, rat aorta embryonic A7R5 cells, and breast carcinoma MCF7 cells (caspase-3 deficient). Different oxysterols, present in large quantity in atheromatous lesions, were used: 7-cétocholestérol (7KC), 7Β-hydroxycholestérol, 25-hydroxycholestérol, cholestérol-5Α, 6Α-ep…

AthéroscléroseCell DeathApoptose[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyLipidesApoptosisOxystérolsAtherosclerosisLipidsPhospholipidosisPhospholipidose<br />Vitamine-ECaspase-2[ SDV.BBM.BC ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Mort cellulaireVitamin E[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM][SDV.BC] Life Sciences [q-bio]/Cellular Biology
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Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ?accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. "Regulated cell death" (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to…

Biochemical Manifestations of Cell DeathISCHEMIA-REPERFUSION INJURYApoptosisReviewTransduction (genetics)0302 clinical medicineCASPASE INHIBITION SWITCHESAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction610 Medicine &amp; healthCaspaseTUMOR-NECROSIS-FACTOR0303 health sciencesSettore BIO/17biologySettore BIO/11NeurodegenerationSettore BIO/13APOPTOSIS3. Good healthMedicina Básicacell death030220 oncology & carcinogenesiscell death; Morphologic Aspects of Cell Death; Biochemical Manifestations of Cell DeathSignal transductionDOMAIN-LIKE PROTEINIntracellularHumanSignal TransductionNecroptosiCYTOCHROME-C RELEASEOUTER-MEMBRANE PERMEABILIZATIONProgrammed cell deathCIENCIAS MÉDICAS Y DE LA SALUDSettore BIO/06Inmunología610 Medicine & healthCELL DEATHNOQ-VD-OPH03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEddc:570Terminology as TopicAPOPTOSIS-INDUCING FACTORMIXED LINEAGE KINASEmedicineAnimalsHumansAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction; Molecular Biology; Cell BiologyMorphologic Aspects of Cell DeathSettore BIO/10Molecular Biology030304 developmental biologyAnimalCell growthApoptosiBiology and Life SciencesCell Biologymedicine.diseaseMITOCHONDRIAL PERMEABILITY TRANSITIONApoptosisImmunologybiology.proteinNeuroscienceCell death and differentiation
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Exercise and Metformin Intervention Prevents Lipotoxicity-Induced Hepatocyte Apoptosis by Alleviating Oxidative and ER Stress and Activating the AMPK…

2022

Objective. Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2DM) commonly coexist and act synergistically to drive adverse clinical outcomes. This study is aimed at investigating the effects of exercise intervention and oral hypoglycaemic drug of metformin (MET) alone or combined on hepatic lipid accumulation. To investigate if oxidative stress and endoplasmic reticulum stress (ERS) are involved in lipotoxicity-induced hepatocyte apoptosis in diabetic mice and whether exercise and/or MET alleviated oxidative stress or ERS-apoptosis by AMPK-Nrf2-HO-1 signaling pathway. Methods. Forty db/db mice with diabetes ( random   blood   glucose ≥ 250   mg / dL ) were randomly allocated i…

Blood GlucoseAgingArticle SubjectNF-E2-Related Factor 2metformiiniApoptosisAMP-Activated Protein KinasesBiochemistryAntioxidantsDiabetes Mellitus ExperimentalMiceohjelmoitunut solukuolemaSuperoxide Dismutase-1aineenvaihduntahäiriötAnimalsHypoglycemic AgentsHematoxylinoksidatiivinen stressibcl-2-Associated X ProteinCaspase 3Cell BiologyGeneral MedicineEndoplasmic Reticulum StressLipidsMetforminOxidative StressDiabetes Mellitus Type 2ei-alkoholiperäinen rasvamaksasairausHepatocyteslääkehoitoEosine Yellowish-(YS)koe-eläinmallitaikuistyypin diabetesSignal TransductionliikuntahoitoOxidative Medicine and Cellular Longevity
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Beneficial Effect of Docosahexanoic Acid and Lutein on Retinal Structural, Metabolic, and Functional Abnormalities in Diabetic Rats

2009

To assess the effect of docosahexanoic acid (DHA) and lutein (both compounds with anti-inflammatory and antioxidant properties) on experimental diabetic retinopathy.Male Wistar rats were studied: non-diabetic controls, untreated diabetic controls, and diabetic rats were treated with DHA and lutein or the combination of DHA + insulin and lutein + insulin for 12 weeks. Oxidative stress and inflammatory markers, apoptosis, and functional tests were studied to confirm biochemical and functional changes in the retina of diabetic rats. Malondialdehyde (MDA), glutathione concentrations (GSH), and glutathione peroxidase activity (GPx) were measured as oxidative stress markers. TUNEL assay and caspa…

Blood GlucoseMaleLuteingenetic structuresmedicine.medical_treatmentApoptosismedicine.disease_causeAntioxidantschemistry.chemical_compoundMalondialdehydeInsulinFluorescent Antibody Technique Indirectchemistry.chemical_classificationCaspase 3NitrotyrosineGlutathione peroxidaseAnti-Inflammatory Agents Non-Steroidalfood and beveragesMalondialdehydeGlutathioneSensory SystemsDrug Therapy Combinationmedicine.medical_specialtyDocosahexaenoic AcidsEnzyme-Linked Immunosorbent AssayBiologyRetinaDiabetes Mellitus ExperimentalCellular and Molecular NeuroscienceDiabetes mellitusInternal medicineElectroretinographyIn Situ Nick-End LabelingmedicineAnimalsRats WistarGlutathione PeroxidaseDiabetic RetinopathyInsulinLuteinGlutathionemedicine.diseaseeye diseasesRatsOxidative StressOphthalmologyEndocrinologychemistryTyrosinesense organsBiomarkersOxidative stressCurrent Eye Research
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Caspase-dependent cell death involved in brain damage after acute subdural hematoma in rats

2006

Abstract Traumatic brain injury is associated with acute subdural hematoma (ASDH) that worsens outcome. Although early removal of blood can reduce mortality, patients still die or remain disabled after surgery and additional treatments are needed. The blood mass and extravasated blood induce pathomechanisms such as high intracranial pressure (ICP), ischemia, apoptosis and inflammation which lead to acute as well as delayed cell death. Only little is known about the basis of delayed cell death in this type of injury. Thus, the purpose of the study was to investigate to which extent caspase-dependent intracellular processes are involved in the lesion development after ASDH in rats. A volume o…

Brain InfarctionMalePathologymedicine.medical_specialtyTraumatic brain injuryIschemiaApoptosisBrain damageNeuroprotectionAmino Acid Chloromethyl KetonesBrain IschemiaRats Sprague-DawleyLesionIn Situ Nick-End LabelingmedicineAnimalsHematoma Subdural AcuteEnzyme InhibitorsSubdural spaceMolecular BiologyIntracranial pressurebusiness.industryVascular diseaseGeneral Neurosciencemedicine.diseaseRatsDisease Models AnimalBloodNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureBrain InjuriesCaspasesAnesthesiaNeurology (clinical)Intracranial Hypertensionmedicine.symptombusinessSignal TransductionDevelopmental BiologyBrain Research
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CD95 DISC formation and internalizzation occur in lipid rafts of typeI and typeII cells

2004

We investigated the membrane localization of CD95 in type I and type II cells, which differ in their ability to recruit and activate caspase-8. We found that CD95 was preferentially located in lipid rafts of type I cells, while it was present both in raft and non-raft plasma membrane sub-domains of type II cells. After stimulation, CD95 located in phospholipid-rich plasma membrane was recruited to lipid rafts in both types of cells. Similarly, CD95 cross-linking resulted in caspase-independent translocation of FADD/MORT1 and caspase-8 to the lipid rafts, which was prevented by a death domain-defective receptor. CD95 internalization was then rapid in type I and delayed in type II cells and s…

CD95Caspase-8Lipid rafts
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Caspase-1 involvement in colorectal cancer cell death phenomenons

2014

Colon cancer is a major public health matter because it has reached the second rank of cancer mortality in 2013 in France. Surgery, radiotherapy and standard chemotherapies helped by targeted therapies are not often efficient enough, underlying the need of using new therapies.Against this background, we have studied the possibilities to use new therapies (Liver X Receptor (LXR) ligands) or to improve classical treatment conditions (hyperthermic intraperitoneal chemotherapy (HIPC)) and the implication of caspase-1.We have first demonstrated that the nuclear receptor (LXR) agonists can induce pyroptotic cell death of colon cancer cell lines by inflammasome activation and subsequent caspase-1 …

CHIPCaspase-1LXRCancer coliqueOxystérolsPyroptose[SDV.BC] Life Sciences [q-bio]/Cellular Biology
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Mir-675-5p supports hypoxia-induced drug resistance in colorectal cancer cells.

2022

Abstract Background The uncontrolled proliferation of cancer cells determines hypoxic conditions within the neoplastic mass with consequent activation of specific molecular pathways that allow cells to survive despite oxygen deprivation. The same molecular pathways are often the cause of chemoresistance. This study aims to investigate the role of the hypoxia-induced miR-675-5p in 5-Fluorouracil (5-FU) resistance on colorectal cancer (CRC) cells. Methods CRC cell lines were treated with 5-Fu and incubated in normoxic or hypoxic conditions; cell viability has been evaluated by MTT assay. MiR-675-5p levels were analysed by RT-PCR and loss and gain expression of the miRNA has been obtained by t…

Cancer Research5-fluorouracil (5-FU)Caspase 3MicroRNAApoptosisGene Expression Regulation NeoplasticColorectal cancer (CRC)MicroRNAsOncologyDrug Resistance NeoplasmDrug resistanceCell Line TumorGeneticsHumansFluorouracilColorectal NeoplasmsHypoxiaBMC cancer
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SAHA induces apoptosis in hepatoma cells and synergistically interacts with the proteasome inhibitor Bortezomib.

2007

Histone deacetylase (HDAC) inhibitors represent a promising group of anticancer agents. This paper shows that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) stimulated at 5-10 microM apoptosis in human hepatoma HepG2 and Huh6 cells, but was ineffective in primary human hepatocytes (PHH). In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8. Moreover, SAHA enhanced the level of Bim proteins, stimulated alternative splicing of the Bcl-X transcript with the expression of the proapoptotic Bcl-Xs isoform, induced degradation of Bid into the apoptotic factor t-Bid and dephosphorylat…

Cancer ResearchCarcinoma HepatocellularFas Ligand ProteinClinical BiochemistryPharmaceutical ScienceApoptosisHydroxamic AcidsFas ligandHistone DeacetylasesBortezomibCell Line TumormedicineHumansProtease InhibitorsProtein kinase BVorinostatHDAC inhibitors . HepG2 cells . PHH . Extrinsic and intrinsic apoptotic pathwaysbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialCaspase 8VorinostatbiologyChemistryBortezomibCytochrome cBiochemistry (medical)Cell BiologyBoronic AcidsHistone Deacetylase InhibitorsProteasomeApoptosisPyrazinesProteasome inhibitorbiology.proteinCancer researchApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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