Search results for "Programmed cell death"

showing 10 items of 609 documents

Cucurbitacins as inducers of cell death and a rich source of potential anticancer compounds.

2011

Triterpenes have been reported to induce cell death. One relevant group of this family of compounds is cucurbitacins, which have been studied as inducers of apoptosis in various cancer cell lines. The most significant mechanisms with regard to the apoptotic effects of cucurbitacins are their ability to modify transcriptional activities via nuclear factors or genes and their capability to activate or inhibit pro- or anti-apoptotic proteins. Still, while the majority of studies on these compounds have dealt with their apoptotic effects on cancer cell lines, several research groups have also explored their anti-inflammatory activities. In general, cucurbitacins are considered to be selective i…

PharmacologyMAPK/ERK pathwayProgrammed cell deathCell CycleApoptosisCucurbitacinsCell cycleBiologyAntineoplastic Agents PhytogenicstatCell biologyCucurbitacinsApoptosisDrug Discoverybiology.proteinAnimalsHumansCyclin D3STAT3Signal TransductionCurrent pharmaceutical design
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Enhanced oxidative stress and increased mitochondrial mass during Efavirenz-induced apoptosis in human hepatic cells

2010

BACKGROUND AND PURPOSE Efavirenz (EFV) is widely used in the treatment of HIV-1 infection. Though highly efficient, there is growing concern about EFV-related side effects, the molecular basis of which remains elusive. EXPERIMENTAL APPROACH In vitro studies were performed to address the effect of clinically relevant concentrations of EFV (10, 25 and 50 µM) on human hepatic cells. KEY RESULTS Cellular proliferation and viability were reduced in a concentration-dependent manner. Analyses of the cell cycle and several cell death parameters (chromatin condensation, phosphatidylserine exteriorization, mitochondrial proapoptotic protein translocation and caspase activation) revealed that EFV trig…

PharmacologyMitochondrial DNAProgrammed cell deathMitochondrionBiologymedicine.diseasemedicine.disease_causeCell biologyMitochondrial toxicitychemistry.chemical_compoundchemistryBiochemistryApoptosismedicineCardiolipinOxidative stressMitochondrial DNA replicationBritish Journal of Pharmacology
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Flupirtine increases the levels of glutathione and Bcl-2 in hNT (human ) neurons: mode of action of the drug-mediated anti-apoptotic effect

1996

Flupirtine is a triaminopyridine analogue which has been successfully applied in clinics as a non-opiate analgesic drug. Previously we described that flupirtine acts like an N-methyl-D-aspartate (NMDA) receptor antagonist in neuronal cells both in vitro and in vivo. Here we show that flupirtine displays its anti-apoptotic effect also in hNT (human Ntera/D1) neurons. hNT neurons were induced to apoptosis applying glutamate (Glu; at concentrations > or = 1 mM) or NMDA (> or = 1 mM). During Glu/NMDA-mediated apoptosis the levels of the intracellular anti-apoptotic agents Bc1-2 and glutathione dropped by more than 50%. Flupirtine completely abolished this reduction of Bc1-2 and glutathione leve…

PharmacologyProgrammed cell deathChemistrymedicine.drug_classGlutamate receptorGlutathionePharmacologyReceptor antagonistchemistry.chemical_compoundmedicine.anatomical_structurenervous systemBiochemistryMechanism of actionmedicineNMDA receptorNeuronFlupirtinemedicine.symptommedicine.drugEuropean Journal of Pharmacology
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Apaf-1 deficient mouse fibroblasts are resistant to MNNG and MMS-induced apoptotic death without attenuation of Bcl-2 decline.

2005

Abstract Simple alkylating agents induce cell death by activating the apoptotic pathway. In rodent fibroblasts, apoptosis triggered by DNA methylation lesions is executed via the mitochondrial damage pathway. Here, we studied cell death induced by the methylating agents methyl methanesulfonate (MMS) and N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) in mouse fibroblasts wild-type (wt) and deficient for Apaf-1 (apaf-1 knockout cells). Apaf-1 is an essential component of the apoptosome complex that becomes activated upon cytochrome c release from mitochondria. We show that apaf-1 knockout cells are more resistant to the cytotoxic effect (as measured by WST assay) of methylating agents. This is d…

PharmacologyProgrammed cell deathMethylnitronitrosoguanidineDNA damageCytochrome cApoptosisBiologyToxicologyMethyl MethanesulfonateMolecular biologyMethyl methanesulfonatechemistry.chemical_compoundMiceApoptotic Protease-Activating Factor 1chemistryProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisbiology.proteinCytotoxic T cellAnimalsApoptosomeCell Line TransformedToxicology and applied pharmacology
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Peptides in apoptosis research

2002

Apoptosis is a complex process that plays a central role in physiological and pathological cell death. This fast evolving research area has experienced incredible development in the past few years. Progress in the knowledge of the structure of many of the main molecular actors of the apoptotic signal transduction pathways has driven the design of synthetic peptides that in some cases can function as simplified versions of their parent proteins. These molecules are contributing to a better understanding of the activity and regulation of apoptotic proteins and also are setting the basis for the discovery of effective drugs to combat important diseases related to apoptosis. Most applications o…

PharmacologyProgrammed cell deathbiologyOrganic ChemistryIntrinsic apoptosisGeneral MedicineBiochemistryCell biologyStructural BiologyApoptosisDrug Discoverybiology.proteinMolecular MedicineApoptosomeSignal transductionMolecular BiologyPeptide sequenceCaspaseFunction (biology)Journal of Peptide Science
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Effects of chemically modified tetracyclines (CMTs) in sensitive, multidrug resistant and apoptosis resistant leukaemia cell lines

2001

Recently discovered chemically modified tetracyclines (CMTs) have shown in vitro and in vivo anti-proliferative and anti-tumour activities. Here, we evaluated in vitro the anti-proliferative and apoptotic activity of six different dedimethylamino chemically modified tetracyclines (CMT-1, CMT-3, CMT-5, CMT-6, CMT-7 and CMT-8) in sensitive and multidrug resistant myeloid leukaemia cells (HL60 and HL60R) in vitro. Three of these compounds (CMT-5, CMT-6, CMT-7) showed low cytotoxic activity both in sensitive and in resistant cells, CMT-3 was endowed with a high anti-proliferative activity only in sensitive cells and was moderately effective as apoptosis inducing agent, with an activity similar …

Pharmacologycongenital hereditary and neonatal diseases and abnormalitiesProgrammed cell deathbiologyBiological activitynervous system diseasesMultiple drug resistanceBiochemistryCell cultureApoptosisCancer researchbiology.proteinCytotoxic T cellCaspaseAntibacterial agentBritish Journal of Pharmacology
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Growth hormone protects human lymphocytes from irradiation-induced cell death

2003

1. Undesired effects of cancer radiotherapy mainly affect the hematopoietic system. Growth hormone (GH) participates in both hematopoiesis and modulation of the immune response. We report both r-hGH cell death prevention and restoration of secretory capacities of irradiated human peripheral blood lymphocytes (PBL) in vitro. 2. r-hGH induced cell survival and increased proliferation of irradiated cells. Western blot analysis indicated that these effects of GH were paralleled by increased expression of the antiapoptotic protein Bcl-2. 3. r-hGH restored mitogen-stimulated release of IL-2 by PBL. Preincubation of irradiated lymphocytes with the growth hormone receptor (GHR) antagonists B2036 an…

Pharmacologymedicine.medical_specialtyProgrammed cell deathmedicine.diagnostic_testCellCancerGrowth hormone receptorBiologymedicine.diseaseHaematopoiesisEndocrinologymedicine.anatomical_structureImmune systemWestern blotApoptosisInternal medicinemedicineCancer researchhormones hormone substitutes and hormone antagonistsBritish Journal of Pharmacology
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Cellular Models and Assays to Study NLRP3 Inflammasome Biology

2020

The NLRP3 inflammasome is a multi-protein complex that initiates innate immunity responses when exposed to a wide range of stimuli, including pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). Inflammasome activation leads to the release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 and to pyroptotic cell death. Over-activation of NLRP3 inflammasome has been associated with several chronic inflammatory diseases. A deep knowledge of NLRP3 inflammasome biology is required to better exploit its potential as therapeutic target and for the development of new selective drugs. To this purpose, in the past few years, several tools have…

Programmed cell death2019-20 coronavirus outbreakInflammasomesInterleukin-1betaReviewBiologyBiochemical assaysModels BiologicalCatalysisInflammasomelcsh:ChemistryInorganic ChemistryNLRP3NLR Family Pyrin Domain-Containing 3 ProteinPyroptosismedicineDeep knowledgeAlarminsAnimalsHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyInnate immune systemintegumentary systemCell modelsPathogen-Associated Molecular Pattern MoleculesOrganic ChemistryInterleukin-18InterleukinInflammasomeGeneral MedicineBiophysical assaysImmunity InnateComputer Science ApplicationsCell biologyNLRP3 inhibitorslcsh:Biology (General)lcsh:QD1-999Mechanism of actionRead-outsmedicine.symptomInflammasome complexSignal Transductionmedicine.drugInternational Journal of Molecular Sciences
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The triaminopyridine flupirtine prevents cell death in rat cortical cells induced by N-methyl-D-aspartate and gp120 of HIV-1.

1994

Abstract Flupirtine, a triaminopyridine derivative, is a non-opiate centrally acting analgesic agent with muscle relaxant properties. Now we show that this drug displays a potent cytoprotective effect on neurons (rat cortical cells) treated with (i) the excitatory amino acid N-methyl- d -aspartate (NMDA) or (ii) with the human immunodeficiency virus type 1 (HIV-1) coat protein gp120. In the absence of the drug the two agents cause a >90% reduction of cell viability after a 18 h incubation. During this period the DNA in the cells undergoes fragmentation and shows a pattern which is typical for cell death. If the neurons were preincubated with flupirtine for 2 h and subsequently exposed to th…

Programmed cell deathAIDS Dementia ComplexN-Methylaspartatemedicine.drug_classCell SurvivalAnalgesicAminopyridinesBiologyPharmacologyHIV Envelope Protein gp120medicineAnimalsViability assayFragmentation (cell biology)Rats WistarCells CulturedPharmacologyCerebral CortexNeuronsAnalgesicsCell DeathMuscle relaxantRatsMolecular Weightmedicine.anatomical_structureImmunologyHIV-1NMDA receptorNeuronFlupirtinemedicine.drugEuropean journal of pharmacology
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The unsolved relationship of brain aging and late-onset Alzheimer disease.

2009

Late-onset Alzheimer disease is the most common form of dementia and is strongly associated with age. Today, around 24 million people suffer from dementia and with aging of industrial populations this number will significantly increase throughout the next decades. An effective therapy that successfully decelerates or prevents the progressive neurodegeneration does not exist. Histopathologically Alzheimer disease is characterized by extensive extracellular amyloid beta (Abeta) plaques, intracellular neurofibrillary tangles (NFTs), synaptic loss and neuronal cell death in distinct brain regions. The molecular correlation of Abeta or NFTs and development of late-onset Alzheimer disease needs f…

Programmed cell deathAgingAmyloid βFree RadicalsBiophysicsmedicine.disease_causeBiochemistryModels BiologicalAtrophyAlzheimer DiseasemedicineExtracellularDementiaAnimalsHumansMolecular BiologyAmyloid beta-Peptidesbusiness.industryBrainNeurodegenerative Diseasesmedicine.diseaseDementiaAlzheimer's diseasebusinessNeuroscienceOxidative stressIntracellularBiochimica et biophysica acta
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