Search results for "CHON"

showing 10 items of 1866 documents

Evaluation of Long-Time Decoction-Detoxicated Hei-Shun-Pian (Processed Aconitum carmichaeli Debeaux Lateral Root With Peel) for Its Acute Toxicity an…

2020

Background As a degenerative joint disease with severe cartilage destruction and pain, osteoarthritis (OA) has no satisfactory therapy to date. In traditional Chinese medicine (TCM), Aconitum carmichaeli Debeaux derived Hei-shun-pian (Hsp) has been developed for joint pain treatment. However, it causes adverse events in OA patients. Long-time decoction has been traditionally applied to reduce the aconite toxicity of Hsp and other aconite herbs, but its detoxifying effect is uncertain. Methods Hsp was extracted with dilute decoction times (30, 60, and 120 min) and evaluated by toxicological, chemical, pharmacological assays. Acute toxicity assay and chemical analysis were employed to determi…

0301 basic medicineChondrocyte hypertrophyDecoctionOsteoarthritisPharmacology03 medical and health scienceschemistry.chemical_compoundtraditional Chinese medicine0302 clinical medicineTherapeutic indexAconitum carmichaeliMedicineAconitinePharmacology (medical)Viability assayOriginal ResearchPharmacologybusiness.industrylcsh:RM1-950monosodium iodoacetateanalgesiapain behaviourmedicine.diseaseAcute toxicityosteoarthritis030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisToxicitybusinessFrontiers in Pharmacology
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The potential of aldehyde dehydrogenase 2 as a therapeutic target in cardiovascular disease.

2018

Mitochondrial aldehyde dehydrogenase (ALDH-2) plays a major role in the ethanol detoxification pathway by removing acetaldehyde. Therefore, ALDH-2 inhibitors such as disulfiram represent the first therapeutic targeting of ALDH-2 for alcoholism therapy. Areas covered: Recently, ALDH-2 was identified as an essential bioactivating enzyme of the anti-ischemic organic nitrate nitroglycerin, bringing ALDH-2 again into the focus of clinical interest. Mechanistic studies on the nitroglycerin bioactivation process revealed that during bioconversion of nitroglycerin and in the presence of reactive oxygen and nitrogen species the active site thiols of ALDH-2 are oxidized and the enzyme activity is los…

0301 basic medicineClinical BiochemistryAldehyde dehydrogenasemedicine.disease_causeAntioxidants03 medical and health scienceschemistry.chemical_compoundDetoxificationDrug DiscoverymedicineAnimalsHumansMolecular Targeted TherapyPharmacologyEthanolbiologyAldehyde Dehydrogenase MitochondrialMitochondrial Aldehyde DehydrogenaseAcetaldehydeCardiovascular AgentsDisease Models AnimalOxidative Stress030104 developmental biologyBiochemistrychemistryCardiovascular DiseasesDrug DesignCardiovascular agentDisulfirambiology.proteinMolecular MedicineOxidative stressmedicine.drugExpert opinion on therapeutic targets
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Enhanced autophagic-lysosomal activity and increased BAG3-mediated selective macroautophagy as adaptive response of neuronal cells to chronic oxidati…

2019

Oxidative stress and a disturbed cellular protein homeostasis (proteostasis) belong to the most important hallmarks of aging and of neurodegenerative disorders. The proteasomal and autophagic-lysosomal degradation pathways are key measures to maintain proteostasis. Here, we report that hippocampal cells selected for full adaptation and resistance to oxidative stress induced by hydrogen peroxide (oxidative stress-resistant cells, OxSR cells) showed a massive increase in the expression of components of the cellular autophagic-lysosomal network and a significantly higher overall autophagic activity. A comparative expression analysis revealed that distinct key regulators of autophagy are upregu…

0301 basic medicineClinical BiochemistryLFQ Label-free quantificationLETM Leucine zipper and EF-hand containing transmembrane proteinmedicine.disease_causeBiochemistryCHX Cycloheximide0302 clinical medicineBNIP3 Bcl-2 interacting protein 3RAPA RapamycinPIK3C3 Class III PI3‐kinasePhosphorylationlcsh:QH301-705.5Neuronslcsh:R5-920PolyUB PolyubiquitinChemistryBAG3OPA1 Optic atrophy 1TOR Serine-Threonine KinasesWIPI1 WD repeat domain phosphoinositide-interacting protein 1ATG Autophagy relatedTFEB Transcription factor EBCell biologyMitochondriasiRNA Small interfering RNADLP1 Dynamin-like protein 1LAMP1 Lysosomal‐associated membrane protein 1PURO Puromycinlcsh:Medicine (General)Protein homeostasisResearch PaperBafA1 Bafilomycin A1LAMP2 Lysosomal‐associated membrane protein 2Proteasome Endopeptidase ComplexRAB18 Member RAS oncogeneTUB TubulinLC3 Light chain 3 proteinOxidative phosphorylationBAG3CTSD Cathepsin DModels BiologicalCell Line03 medical and health sciencesDownregulation and upregulationMacroautophagymedicineAutophagyHumansAdaptationBAG1 Bcl-2-associated athanogene 1BECN1 Beclin1PI3K/AKT/mTOR pathwayAdaptor Proteins Signal TransducingTEM Transmission electron microscopyHsp70 Heat shock protein 70Organic ChemistryAutophagyAutophagosomesmTOR Mammalian target of rapamycinHsp70Oxidative Stress030104 developmental biologyProteostasislcsh:Biology (General)CV CanavanineBAG3 Bcl-2-associated athanogene 3MTT (3-(45-Dimethylthiazol-2-yl)-25-Diphenyltetrazolium Bromide)Apoptosis Regulatory ProteinsLysosomes030217 neurology & neurosurgeryOxidative stressRedox Biology
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Mitophagy in human astrocytes treated with the antiretroviral drug Efavirenz: Lack of evidence or evidence of the lack

2019

Efavirenz (EFV), a first generation non-nucleoside analogue reverse transcriptase inhibitor widely employed in combination antiretroviral therapy regimens over the last 20 years, has been associated with a wide range of neuropsychiatric effects and has also been linked with HIV-associated neurocognitive disorder (HAND). EFV has been reported to alter mitochondrial dysfunction and bioenergetics in different cell types, including astrocytes. Here, we analyzed whether this mitochondrial effect is associated with alterations in autophagy and, more specifically, mitophagy. U251-MG cells were exposed to EFV (10 and 25 μM; 24 h) and the effect was compared with that of CCCP - an uncoupler of the m…

0301 basic medicineCyclopropanesCell typeThapsigarginEfavirenz030106 microbiologyMitochondrial DegradationBiologyMitochondrionPharmacologyMitochondrial Proteins03 medical and health scienceschemistry.chemical_compoundCitologíaVirologyCell Line TumorMitophagymedicineAutophagyHumansPharmacologyReverse-transcriptase inhibitorBiología celularAutophagyAutophagosomesMitophagyBenzoxazinesMitochondriaAntiretroviral030104 developmental biologychemistryAnti-Retroviral AgentsAlkynesAstrocytesReverse Transcriptase InhibitorsEfavirenzVirologíamedicine.drug
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Mitochondrial BAX Determines the Predisposition to Apoptosis in Human AML

2017

Abstract Purpose: Cell-to-cell variability in apoptosis signaling contributes to heterogenic responses to cytotoxic stress in clinically heterogeneous neoplasia, such as acute myeloid leukemia (AML). The BCL-2 proteins BAX and BAK can commit mammalian cells to apoptosis and are inhibited by retrotranslocation from the mitochondria into the cytosol. The subcellular localization of BAX and BAK could determine the cellular predisposition to apoptotic death. Experimental Design: The relative localization of BAX and BAK was determined by fractionation of AML cell lines and patient samples of a test cohort and a validation cohort. Results: This study shows that relative BAX localization determine…

0301 basic medicineCytoplasmCancer ResearchApoptosisKaplan-Meier EstimateBiologyMitochondrionMitochondrial Proteins03 medical and health sciencesCell Line Tumorhemic and lymphatic diseasesmedicineHumansCytotoxic T cellLeukocytosisRetrospective Studiesbcl-2-Associated X ProteinMyeloid leukemiaCancerRetrospective cohort studymedicine.diseaseMitochondriaProtein TransportLeukemiabcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyOncologyLeukemia MyeloidApoptosisAcute DiseaseImmunologyCancer researchmedicine.symptomHeLa CellsClinical Cancer Research
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Enterocyte Purge and Rapid Recovery Is a Resilience Reaction of the Gut Epithelium to Pore-Forming Toxin Attack.

2016

International audience; Besides digesting nutrients, the gut protects the host against invasion by pathogens. Enterocytes may be subjected to damage by both microbial and host defensive responses, causing their death. Here, we report a rapid epithelial response that alleviates infection stress and protects the enterocytes from the action of microbial virulence factors. Intestinal epithelia exposed to hemolysin, a pore-forming toxin secreted by Serratia marcescens, undergo an evolutionarily conserved process of thinning followed by the recovery of their initial thickness within a few hours. In response to hemolysin attack, Drosophila melanogaster enterocytes extrude most of their apical cyto…

0301 basic medicineCytoplasmDisease toleranceSurvivalApoptosismedicine.disease_causeOral infectionHemolysin ProteinsLipid droplet[SDV.IDA]Life Sciences [q-bio]/Food engineeringMitochondrial extrusionIntestinal MucosaSerratia marcescensBacterial-infectionPore-forming toxinbiologyCell DeathMicrovilliPlasma-membrane[ SDV.IDA ] Life Sciences [q-bio]/Food engineeringGut EpitheliumMitochondriamedicine.anatomical_structureDrosophila melanogasterEnterocyteVirulence FactorsVarroidaeSerratia-marcescensBacterial ToxinsVirulenceMicrobiologyMicrobiologySerratia Infections03 medical and health sciencesVirologymedicineAnimalsApical cytoplasmDefense strategyDrosophila cyclin jToxinbiology.organism_classificationLipid dropletsDisease Models AnimalIntestinal Diseases030104 developmental biologyEnterocytesSerratia marcescensParasitologyDigestive SystemCell hostmicrobe
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Cofilin and Neurodegeneration: New Functions for an Old but Gold Protein

2021

Cofilin is an actin-binding protein that plays a major role in the regulation of actin dynamics, an essential cellular process. This protein has emerged as a crucial molecule for functions of the nervous system including motility and guidance of the neuronal growth cone, dendritic spine organization, axonal branching, and synaptic signalling. Recently, other important functions in cell biology such as apoptosis or the control of mitochondrial function have been attributed to cofilin. Moreover, novel mechanisms of cofilin function regulation have also been described. The activity of cofilin is controlled by complex regulatory mechanisms, with phosphorylation being the most important, since t…

0301 basic medicineDendritic spine organizationCellMotilityNeurosciences. Biological psychiatry. NeuropsychiatryReviewmacromolecular substancescofilinBiologyenvironment and public health03 medical and health sciences0302 clinical medicinemedicineneurodegenerative diseasescofilin–actin rodsGeneral Neurosciencemitochondrial fissionNeurodegenerationapoptosisCofilinmedicine.diseaseCell biologymicrotubule instability030104 developmental biologymedicine.anatomical_structurePhosphorylationMitochondrial fission030217 neurology & neurosurgeryFunction (biology)RC321-571Brain Sciences
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Methylmercury-induced developmental toxicity is associated with oxidative stress and cofilin phosphorylation. Cellular and human studies

2017

Environmental exposure to methylmercury (MeHg) during development is of concern because it is easily incorporated in children’s body both pre- and post-natal, it acts at several levels of neural pathways (mitochondria, cytoskeleton, neurotransmission) and it causes behavioral impairment in child. We evaluated the effects of prolonged exposure to 10–600 nM MeHg on primary cultures of mouse cortical (CCN) and of cerebellar granule cells (CGC) during their differentiation period. In addition, it was studied if prenatal MeHg exposure correlated with altered antioxidant defenses and cofilin phosphorylation in human placentas (n = 12) from the INMA cohort (Spain). Exposure to MeHg for 9 days in v…

0301 basic medicineDevelopmental DisabilitiesGlutathione reductaseCiencias de la SaludMitochondrionMETHYLMERCURYToxicologymedicine.disease_causeProtein CarbonylationMiceCytosolMITOCHONDRIAPregnancyPhosphorylationOXIDATIVE STRESSCells Culturedchemistry.chemical_classificationNeuronsbiologyGeneral NeuroscienceGlutathione peroxidaseCOFILINBrainMethylmercuryEnvironmental exposureCofilinMethylmercury CompoundsMitochondrial Proton-Translocating ATPasesGlutathioneCell biologyMitochondriaGlutathione ReductaseActin Depolymerizing FactorsCofilinPhosphorylationFemaleHuman placentaactinCortactinCIENCIAS MÉDICAS Y DE LA SALUDmacromolecular substancesACTIN03 medical and health sciencesCultured neuronsmedicineAnimalsHumansCULTURED NEURONSGlutathione PeroxidaseSalud OcupacionalHUMAN PLACENTAMolecular biology030104 developmental biologychemistryAnimals NewbornOxidative stressbiology.proteinOxidative stress
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Customised in vitro model to detect human metabolism-dependent idiosyncratic drug-induced liver injury

2017

Drug-induced liver injury (DILI) has a considerable impact on human health and is a major challenge in drug safety assessments. DILI is a frequent cause of liver injury and a leading reason for post-approval drug regulatory actions. Considerable variations in the expression levels of both cytochrome P450 (CYP) and conjugating enzymes have been described in humans, which could be responsible for increased susceptibility to DILI in some individuals. We herein explored the feasibility of the combined use of HepG2 cells co-transduced with multiple adenoviruses that encode drug-metabolising enzymes, and a high-content screening assay to evaluate metabolism-dependent drug toxicity and to identify…

0301 basic medicineDrugCYP2B6Drug-induced liver injuryHealth Toxicology and Mutagenesismedia_common.quotation_subjectPopulationDrug Evaluation PreclinicalPharmacologyToxicologyHepatotoxicity mechanismsGene Expression Regulation EnzymologicOrgan Toxicity and MechanismsAdenoviridae03 medical and health sciences0302 clinical medicineCYPToxicity TestsHumansCytochrome P450 Family 2educationmedia_commonMembrane Potential Mitochondrialeducation.field_of_studyCYP3A4biologyCytochrome P450IdiosyncrasyHep G2 CellsGeneral MedicineCYP2E1Recombinant ProteinsHigh-Throughput Screening Assays030104 developmental biology030220 oncology & carcinogenesisInactivation MetabolicToxicityCell modelbiology.proteinChemical and Drug Induced Liver InjuryReactive Oxygen SpeciesDrug metabolism
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Exercise training as a drug to treat age associated frailty

2016

Exercise causes an increase in the production of free radicals [1]. As a result of a hormetic mechanism antioxidant enzymes are synthesised and the cells are protected against further oxidative stress. Thus, exercise can be considered as an antioxidant [2]. Age-associated frailty is a major medical and social concern as it can easily lead to dependency. In this review we describe that oxidative stress is associated with frailty and the mechanism by which exercise prevents age-associated frailty. We propose that individually tailored multicomponent exercise programmes are one of the best ways to prevent and to treat age-associated frailty.

0301 basic medicineDrugGerontologyAgingmedicine.medical_specialtyRos signallingFree Radicalsmedia_common.quotation_subjectmedicine.disease_causeBiochemistry03 medical and health sciencesPhysiology (medical)HumansMedicineIntensive care medicineExercisemedia_commonFrailtybusiness.industryMechanism (biology)TOR Serine-Threonine KinasesHormesisMitochondriaOxidative Stress030104 developmental biologybusinessOxidative stressFree Radical Biology and Medicine
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