Search results for " Mitogen"

showing 10 items of 202 documents

Toxicity as prime selection criterion among SARS-active herbal medications

2021

We present here a new selection criterion for prioritizing research on efficacious drugs for the fight against COVID-19: the relative toxicity versus safety of herbal medications, which were effective against SARS in the 2002/2003 epidemic. We rank these medicines according to their toxicity versus safety as basis for preferential rapid research on their potential in the treatment of COVID-19. The data demonstrate that from toxicological information nothing speaks against immediate investigation on, followed by rapid implementation of Lonicera japonica, Morus alba, Forsythia suspensa, and Codonopsis spec. for treatment of COVID-19 patients. Glycyrrhiza spec. and Panax ginseng are ranked in …

2019-20 coronavirus outbreakmedicine.medical_specialtyRelative toxicityCoronavirus disease 2019 (COVID-19)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Pharmaceutical ScienceReviewSARS-CoV-2 severe acute respiratory syndrome coronavirus 203 medical and health sciencesCytochrome P450 Phytochemicals0302 clinical medicineSOD superoxide dismutaseDrug DiscoveryMedicineAnimalsHumansOral applicationIKK inhibitor of κB kinase030304 developmental biologyPharmacologyRational phytotherapy0303 health sciencesPublic healthCOVID-19 Coronavirus disease 2019JNK c-Jun N-terminale kinaseNO nitric oxidePlants MedicinalTraditional medicineToxicityACE2 angiotensin converting enzyme 2business.industrySARS-CoV-2Public healthCOVID-19Th2 T helper cells type 2NF-κB nuclear factor- κ B cellsComplementary and alternative medicine030220 oncology & carcinogenesisToxicityMolecular MedicineCYP cytochrome P450 monooxygenaseHIV-1 human immunodeficiency virus 1businessSelection criterionMAPK mitogen-activated protein kinaseDrugs Chinese HerbalPhytomedicine
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Posttranslationally modified proteins as mediators of sustained intestinal inflammation.

2006

Oxidative and carbonyl stress leads to generation of N(epsilon)-carboxymethyllysine-modified proteins (CML-mps), which are known to bind the receptor for advanced glycation end products (RAGE) and induce nuclear factor (NF)-kappaB-dependent proinflammatory gene expression. To determine the impact of CML-mps in vivo, RAGE-dependent sustained NF-kappaB activation was studied in resection gut specimens from patients with inflammatory bowel disease. Inflamed gut biopsy tissue demonstrated a significant up-regulation of RAGE and increased NF-kappaB activation. Protein extracts from the inflamed zones, but not from noninflamed resection borders, caused perpetuated NF-kappaB activation in cultured…

AdultCell ExtractsMaleReceptor for Advanced Glycation End ProductsInflammationBiologyInflammatory bowel diseasep38 Mitogen-Activated Protein KinasesPathology and Forensic MedicineProinflammatory cytokineRAGE (receptor)MiceGlycationhemic and lymphatic diseasesGene expressionmedicineAnimalsCalgranulin BHumansCalgranulin AIntestinal MucosaReceptors ImmunologicReceptorProtein Kinase InhibitorsMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3LysineNF-kappa Bnutritional and metabolic diseasesEndothelial Cellsmedicine.diseaseNFKB1Inflammatory Bowel DiseasesIntestinesDisease Models AnimalImmunologyCancer researchFemalemedicine.symptomProtein Processing Post-TranslationalRegular ArticlesThe American journal of pathology
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Repeated muscle biopsies through a single skin incision do not elicit muscle signaling, but IL-6 mRNA and STAT3 phosphorylation increase in injured m…

2011

To determine if muscle biopsies can be repeated using a single small (5–6 mm) skin incision without inducing immediate MAPK activation or inflammation in the noninjured areas, the phosphorylation of ERK1/2, p38-MAPK, c-Jun NH2-terminal kinases (JNKs), IκBα, IKKα, and signal transducer and activator of transcription 3 (STAT3) was examined concurrent with IL-6 mRNA in six muscle biopsies obtained from the vastus lateralis of five men. Four biopsies were obtained through the same incision (5–6 mm) from the right leg (taken at 0, 30, 123, and 126 min) and another two each from new incisions performed in the left leg (at 31 and 120 min), while the subjects rested supine. The first three biopsie…

AdultMaleSTAT3 Transcription FactorMAPK/ERK pathwaymedicine.medical_specialtyPathologyTime FactorsPhysiologyBiopsyInflammationp38 Mitogen-Activated Protein KinasesQuadriceps MuscleMuscular DiseasesNF-KappaB Inhibitor alphaPhysiology (medical)Internal medicinemedicineHumansRNA MessengerPhosphorylationSTAT3Interleukin 6Mitogen-Activated Protein Kinase 1Analysis of VarianceWound HealingMitogen-Activated Protein Kinase 3Skin incisionbiologyInterleukin-6JNK Mitogen-Activated Protein KinasesIl 6 mrnaI-kappa B KinaseUp-RegulationEndocrinologybiology.proteinSTAT proteinPhosphorylationI-kappa B Proteinsmedicine.symptomSignal TransductionJournal of Applied Physiology
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Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training

2014

This study investigated the effects of vitamin C and E supplementation on acute responses and adaptations to strength training. Thirty-two recreationally strength-trained men and women were randomly allocated to receive a vitamin C and E supplement (1000 mg day(-1) and 235 mg day(-1), respectively), or a placebo, for 10 weeks. During this period the participants' training involved heavy-load resistance exercise four times per week. Muscle biopsies from m. vastus lateralis were collected, and 1 repetition maximum (1RM) and maximal isometric voluntary contraction force, body composition (dual-energy X-ray absorptiometry), and muscle cross-sectional area (magnetic resonance imaging) were measu…

AdultMalemedicine.medical_specialtyJournal ClubPhysiologyStrength trainingMAP Kinase Signaling Systemmedicine.medical_treatmentMolecular and CellularMuscle ProteinsIsometric exerciseAscorbic AcidBiologyp38 Mitogen-Activated Protein KinasesMuscle hypertrophyIsometric ContractionInternal medicinemedicineHumansVitamin Eta315Leg pressMuscle SkeletalMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Vitamin Cta1184Vitamin EBiceps curlRibosomal Protein S6 Kinases 70-kDaResistance TrainingVitaminsAscorbic acidAdaptation PhysiologicalEndocrinologyDietary SupplementsFemale
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Lipocalin-2 Regulates Hippocampal Microglial Activation in Poststroke Depression

2021

Background and Purpose: Microglia play important role in poststroke depression (PSD), however, the exact mechanism was still unclear. The purpose of the study was to study the mechanism of microglial activation in PSD.Methods: 24 rats were randomly divided into three groups: the PSD group (n = 10), the poststroke (PS) group (n = 7), and the sham group (n = 7). Primary hippocampal microglia were isolated and cultured, and recombined LCN2 protein was used to stimulate the cultured microglia. The protein expression of Iba1, P38 MAPK and PP38 MAPK was analyzed by western blotting; the LCN2 expression was measured by RT-qPCR, the serum LCN2 level and the NO level were analyzed by ELISA.Results: …

Agingpoststroke depression (PSD)nervous systemCognitive NeuroscienceAging NeurosciencemicrogliahippocampiLipocalin-2 (Lcn2)Neurosciences. Biological psychiatry. Neuropsychiatryp38 mitogen-activated protein kinase (p38 MAPK)psychological phenomena and processesOriginal ResearchRC321-571Frontiers in Aging Neuroscience
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Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
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Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression.

1999

Activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases is an early response of cells upon exposure to DNA-damaging agents. JNK-mediated phosphorylation of c-Jun is currently understood to stimulate the transactivating potency of AP-1 (e.g., c-Jun/c-Fos; c-Jun/ATF-2), thereby increasing the expression of AP-1 target genes. Here we show that stimulation of JNK1 activity is not a general early response of cells exposed to genotoxic agents. Treatment of NIH 3T3 cells with UV light (UV-C) as well as with methyl methanesulfonate (MMS) caused activation of JNK1 and an increase in c-Jun protein and AP-1 binding activity, whereas antineoplastic drugs such as mafosfamide, mito…

Alkylating AgentsProto-Oncogene Proteins c-junUltraviolet RaysStimulationBiologyenvironment and public healthWortmanninTransactivationchemistry.chemical_compoundMiceAnimalsPhosphatidylinositolCollagenasesProtein kinase AMolecular BiologyCell Growth and DevelopmentMitogen-Activated Protein Kinase 1Kinasec-junJNK Mitogen-Activated Protein KinasesCell Biology3T3 CellsMethyl MethanesulfonateMolecular biologyAndrostadienesEnzyme ActivationGene Expression Regulation NeoplasticTranscription Factor AP-1chemistryCalcium-Calmodulin-Dependent Protein KinasesPhosphorylationMitogen-Activated Protein KinasesWortmanninMolecular and cellular biology
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Detection of mitochondrial electron chain carrier redox status by transhepatic light intensity during rat liver reperfusion.

2003

The aim of the study was to investigate mitochondrial electron transfer during rat liver reperfusion after cold storage and hypothermic machine perfusion. Livers from male Brown Norway rats were preserved (UW) for 10h either by cold storage (CS) or by hypothermic oxygenated perfusion extracorporal (HOPE). Transhepatic photometric analysis allowed determination of the redox status of mitochondrial cytochromes during preservation, rewarming and reperfusion. Mitochondrial electron chain carriers were inhibited at different sites with rotenone and cyanide in some experiments. reversed transcriptional polymerase chain reaction (RT-PCR) was performed after reperfusion concerning transcription of …

AnionsMaleTime FactorsCytochromeLightCold storageCaspase 3ElectronsDNA FragmentationMitochondrionGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundSuperoxidesAnimalsCaspase-9CryopreservationCyanidesbiologySuperoxideCaspase 3Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaJNK Mitogen-Activated Protein KinasesTemperatureNADH DehydrogenaseGeneral MedicineRotenoneDNAOrgan PreservationLipid MetabolismCaspase 9MitochondriaRatsCold TemperatureOxygenLight intensitychemistryBiochemistryElectron Transport Chain Complex ProteinsLiverCaspasesReperfusionbiology.proteinCytochromesLipid PeroxidationMitogen-Activated Protein KinasesGeneral Agricultural and Biological SciencesReactive Oxygen SpeciesOxidation-ReductionCryobiology
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Mycobacterial antigen(s) induce anergy by altering TCR- and TCR/CD28-induced signalling events: insights into T-cell unresponsiveness in leprosy.

2009

Present study investigates the role of Mycobacterium leprae (M. leprae) antigens on TCR- and TCR/CD28-induced signalling leading to T-cell activation and further correlates these early biochemical events with T-cell anergy, as prevailed in advanced stages of leprosy. We observed that both whole cell lystae (WCL) and soluble fraction of M. leprae sonicate (MLSA) not only inhibited TCR, thapsigargin and ionomycin induced calcium fluxes by diminishing the opening of calcium channels, but also TCR- or TCR/CD28-induced proximal signalling events like phosphorylation of Zap-70 and protein kinase-C (PKC) activity. Study of TCR- and TCR/CD28-induced downstream signals revealed that M. leprae antige…

Antigens Differentiation T-LymphocyteMAP Kinase Signaling SystemT cellT-LymphocytesImmunologyReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyLymphocyte ActivationJurkat cellsp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundJurkat CellsCD28 AntigensAntigens CDLeprosyCalcium fluxmedicineHumansLectins C-TypeEnzyme InhibitorsPromoter Regions GeneticMolecular BiologyMycobacterium lepraeProtein Kinase CCell ProliferationClonal AnergyAntigens BacterialMitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinaseIonophoresNFATC Transcription FactorsIonomycinT-cell receptorInterleukin-2 Receptor alpha SubunitCD28hemic and immune systemsNFATbiology.organism_classificationCell biologyMycobacterium lepraemedicine.anatomical_structurechemistryGene Expression RegulationIonomycinImmunologyInterleukin-2ThapsigarginCalciumMolecular immunology
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To the research of treatments for the typical calcific disease of old aortic valve in the omics era: Is the miR-195 a therapeutic signature via targe…

2020

Calcific aortic valve disease (CAVD) is the most frequent form of val-vular pathology [1,2], with high percentages of mortality and morbidityin Western populations, so much to be a very public health problem [2].Diverse millions of subjects are affected by CAVD and the major numberare old individuals (65- older), even if some have a younger age and aregenerally affected by congenital bicuspid aortic valve (BAV) disease[2,3]. CAVD in BAV individuals arises decades earlier respect to subjectswith the physiological tricuspid aortic valve [3]. Furthermore, it can leadto death if untreated with surgical aortic valve replacement or trans-catheter aortic valve implantation, its unique treatments […

Aortic valvemedicine.medical_specialtybicuspid aortic valvebusiness.industryp38 mitogen-activated protein kinasesDiseasemedicine.diseaseOmicsBicuspid aortic valvemedicine.anatomical_structuremiR-195Internal medicinemedicineCardiologyCardiology and Cardiovascular Medicinebusiness
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