Search results for "tumor necrosis factor-alpha"

showing 10 items of 504 documents

Conditioned Media from Adipose-Tissue-Derived Mesenchymal Stem Cells Downregulate Degradative Mediators Induced by Interleukin-1β in Osteoarthritic C…

2013

Osteoarthritis (OA) is the most frequent joint disorder and an important cause of disability. Recent studies have shown the potential of adipose-tissue-derived mesenchymal stem cells (AD-MSC) for cartilage repair. We have investigated whether conditioned medium from AD-MSC (CM) may regulate in OA chondrocytes a number of key mediators involved in cartilage degeneration. CM enhanced type II collagen expression in OA chondrocytes while decreasing matrix metalloproteinase (MMP) activity in cell supernatants as well as the levels of MMP-3 and MMP-13 proteins and mRNA in OA chondrocytes stimulated with interleukin- (IL-) 1β. In addition, CM increased IL-10 levels and counteracted the stimulating…

MaleArticle Subjectmedicine.medical_treatmentImmunologyInterleukin-1betaType II collagenAdipose tissueDown-RegulationNitric OxideChondrocytesMatrix Metalloproteinase 13Osteoarthritislcsh:PathologymedicineHumansProstaglandin E2Interleukin 6Collagen Type IICells CulturedAgedbiologyChemistryInterleukin-6Tumor Necrosis Factor-alphaMesenchymal stem cellNF-kappa BInterleukinMesenchymal Stem CellsCell BiologyMiddle AgedCell biologyAdipose TissueCulture Media ConditionedImmunologybiology.proteinTumor necrosis factor alphaFemaleMatrix Metalloproteinase 3Inflammation Mediatorslcsh:RB1-214Prostaglandin Emedicine.drugResearch Article
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Effect of autologous blood transfusion on cerebral cytokine expression.

2011

BACKGROUND: Autologous blood transfusion (ABT), for example, by means of cell saver equipment, is used to reduce the need for allogenic blood transfusion in patients with high perioperative blood loss. This study investigated the effect of blood/extracorporal surface interaction during withdrawal and retransfusion of shed autologous blood on cerebral inflammation in rats. Rats subjected to hypotension with cerebral ischemia served as positive controls. METHODS: Eighty-eight male Sprague-Dawley rats were anesthetized with sevoflurane, instrumented, and randomly assigned to the following groups: sham-operation (SHAM), autologous blood withdrawal/transfusion only (ABT), or bilateral carotid ar…

MaleBlood transfusionmedicine.medical_treatmentInterleukin-1betaIschemiaNitric Oxide Synthase Type IIInflammationPharmacologySevofluraneRats Sprague-DawleyBlood Transfusion AutologousmedicineHippocampus (mythology)AnimalsInterleukin 6biologybusiness.industryInterleukin-6Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaBrainmedicine.diseaseRatsNitric oxide synthaseAnesthesiology and Pain MedicineCyclooxygenase 2biology.proteinCytokinesSurgeryTumor necrosis factor alphaNeurology (clinical)medicine.symptombusinessmedicine.drugFollow-Up StudiesJournal of neurosurgical anesthesiology
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Paracrine in vivo inhibitory effects of adipose tissue–derived mesenchymal stromal cells in the early stages of the acute inflammatory response

2015

Abstract Background aims Excessive or unresolved inflammation leads to tissue lesions. Adipose tissue–derived mesenchymal stromal cells (AMSCs) have shown protective effects that may be dependent on the modulation of inflammation by secreted factors. Methods We used the zymosan-induced mouse air pouch model at two time points (4 h and 18 h) to evaluate the in vivo effects of AMSCs and their conditioned medium (CM) on key steps of the early inflammatory response. We assessed the effects of AMSCs and CM on leukocyte migration and myeloperoxidase activity. The levels of chemokines, cytokines and eicosanoids in exudates were measured by use of enzyme-linked immunoassay or radio-immunoassay. In …

MaleCancer ResearchChemokineLeukocyte migrationLeukotriene B4medicine.medical_treatmentInterleukin-1betaImmunologyFluorescent Antibody TechniqueAdipose tissueEnzyme-Linked Immunosorbent AssayInflammationMesenchymal Stem Cell TransplantationLeukotriene B4DinoprostoneMiceParacrine signallingchemistry.chemical_compoundCell MovementParacrine CommunicationLeukocytesmedicineAnimalsImmunology and AllergyGenetics (clinical)Prostaglandin-E SynthasesInflammationTransplantationbiologyInterleukin-6Tumor Necrosis Factor-alphaTranscription Factor RelAZymosanMesenchymal Stem CellsCell BiologyIntramolecular OxidoreductasesAdipose TissueOncologychemistryCyclooxygenase 2Culture Media ConditionedImmunologyCancer researchbiology.proteinCytokinesTumor necrosis factor alphamedicine.symptomProstaglandin ECytotherapy
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Tea catechins induce crosstalk between signaling pathways and stabilize mast cells in ulcerative colitis

2017

It is well documented that nutraceuticals, in general, and Green tea catechins, in particular, possess a potential therapeutic value in inflammatory bowel diseases (IBD) due to their anti-oxidative and anti-inflammatory effects. This study aimed to investigate the possible mechanism of action of catechins in a rat model of colitis induced by 2.4.6 trinitrobenzene sulfonic acid (TNBS). Thirty-five young adult Sprague-Dawley rats were divided into four groups: normal control (n=5), catechins (n=9), TNBS (n=9) and TNBS plus catechins (n=12) treated. Catechin in the form of Epigallocatechin-3-gallate (EGCG) was administered daily by intraperitoneal injection, 1 week before the induction date of…

MaleCancer ResearchColonPhysiologyEndocrinology Diabetes and MetabolismImmunologyAnti-Inflammatory AgentsAntioxidantsCatechinRats Sprague-DawleyEndocrinologyPhysiology (medical)AnimalsImmunology and AllergyMast CellsTeaInterleukin-6Tumor Necrosis Factor-alphaNF-kappa BColitisRatsGene Expression RegulationTrinitrobenzenesulfonic AcidOncologyReactive Oxygen SpeciesSignal Transduction
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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In vivo and in vitro induction of natural killer cells by cloned human tumor necrosis factor

1988

The natural killer (NK) cell activity of mice in the peritoneal cavity is very low or undetectable and testing peritoneal NK cells is a useful model for studying the influence of activating substances upon local injection. Injection of tumor necrosis factor (TNF) at doses of 10-200 ng caused a marked activation of NK cell activity which was maximal after 24 h and declined rapidly on day 2. A similar effect was observed when interferons alpha and beta were injected, and there were additive results when interferon was injected together with TNF. The NK cell nature of the effector cells activated by TNF was substantiated by the finding that previous injection with anti-asialo GM 1 antibody pre…

MaleCancer ResearchNecrosisLymphocyteImmunologyIn Vitro TechniquesBiologyNatural killer cellMiceInterferonmedicineAnimalsImmunology and AllergyCytotoxic T cellMice Inbred C3HLymphokine-activated killer cellTumor Necrosis Factor-alphaMacrophagesMolecular biologyKiller Cells NaturalMice Inbred C57BLmedicine.anatomical_structureOncologyImmunologyInterleukin 12Tumor necrosis factor alphaInterferonsmedicine.symptommedicine.drugCancer Immunology Immunotherapy
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Oncogene-driven intrinsic inflammation induces leukocyte production of tumor necrosis factor that critically contributes to mammary carcinogenesis.

2010

Abstract Oncogene activation promotes an intrinsic inflammatory pathway that is crucial for cancer development. Here, we have investigated the actual effect of the inflammatory cytokine tumor necrosis factor (TNF) on the natural history of spontaneous mammary cancer in the HER2/neuT (NeuT) transgenic mouse model. Bone marrow transplantation from TNF knockout mice into NeuT recipients significantly impaired tumor growth, indicating that the source of TNF fostering tumor development was of bone marrow origin. We show that the absence of leukocyte-derived TNF disarranged the tumor vasculature, which lacked pericyte coverage and structural integrity, leading to diffuse vascular hemorrhage and s…

MaleCancer ResearchStromal cellmedicine.medical_treatmentInflammationmedicine.disease_causeAntibodiesArticleMicemedicineLeukocytesAnimalsHumansReceptors Tumor Necrosis Factor Type IItumor necrosis factor mammary carcinogenesis.Crosses GeneticBone Marrow TransplantationInflammationMice KnockoutOncogenebusiness.industryTumor Necrosis Factor-alphaCancerMammary Neoplasms ExperimentalOncogenesmedicine.diseaseImmunohistochemistryMice Inbred C57BLPlatelet Endothelial Cell Adhesion Molecule-1medicine.anatomical_structureCytokineOncologyReceptors Tumor Necrosis Factor Type IImmunologyTumor necrosis factor alphaFemaleBone marrowmedicine.symptomCarcinogenesisbusinessCancer research
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Erythropoietin for the treatment of anemia of malignancy associated with neoplastic bone marrow infiltration.

1990

This clinical trial was performed to study the effects of intravenously (IV) administered recombinant human (rh) erythropoietin (EPO) at escalating doses (150, 300, and 450 U/kg, administered as an IV bolus injection, twice weekly, for 6, 4, and 4 weeks, respectively) in five patients with low-grade non-Hodgkin's lymphoma (Ig NHL) and bone marrow involvement and one patient with multiple myeloma (MM). All patients were anemic due to underlying disease. None of the patients had a history of bleeding, hemolysis, renal insufficiency, or other disorders causing anemia in addition to bone marrow infiltrating malignancy. Endogenous EPO serum levels were significantly increased in all patients (7…

MaleCancer Researchmedicine.medical_specialtyAnemiaHematocritMalignancyGastroenterologyBone Marrowhemic and lymphatic diseasesInternal medicineNeoplasmsMedicineHumansErythropoiesisBlood CoagulationErythropoietinMultiple myelomaAgedClinical Trials as Topicmedicine.diagnostic_testbusiness.industryTumor Necrosis Factor-alphaAnemiaMiddle Agedmedicine.diseaseLymphomaHematopoiesisKineticsmedicine.anatomical_structureOncologyErythropoietinImmunologyFerritinsErythropoiesisFemaleBone marrowbusinessmedicine.drugJournal of clinical oncology : official journal of the American Society of Clinical Oncology
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Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats.

2020

Minimal hepatic encephalopathy is associated with changes in the peripheral immune system which are transferred to the brain, leading to neuroinflammation and thus to cognitive and motor impairment. Mechanisms by which changes in the immune system induce cerebral alterations remain unclear. Extracellular vesicles (EVs) seem to play a role in this process in certain pathologies. The aim of this work was to assess whether EVs play a role in the induction of neuroinflammation in cerebellum and motor incoordination by chronic hyperammonemia. We characterized the differences in protein cargo of EVs from plasma of hyperammonemic and control rats by proteomics and Western blot. We assessed whether…

MaleCerebellumtnfαhepatic encephalopathyArticleExtracellular VesiclesImmune systemWestern blotmedicineAnimalsHumansHyperammonemiaRats WistarReceptorlcsh:QH301-705.5NeuroinflammationInflammationMicrogliamedicine.diagnostic_testbusiness.industryTumor Necrosis Factor-alphaHyperammonemiaGeneral Medicinetnfα receptor tnfr1medicine.diseaseRatsMotor Skills DisordersDisease Models Animalmedicine.anatomical_structurelcsh:Biology (General)glial activationTumor necrosis factor alphaNervous System DiseasesTNF alpha receptor TNFR1businessNeuroscienceTNF alpha
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Bacteria-Derived Compatible Solutes Ectoine and 5α-Hydroxyectoine Act as Intestinal Barrier Stabilizers to Ameliorate Experimental Inflammatory Bowel…

2015

Earlier studies showed that the compatible solute ectoine (1) given prophylactically before induction of colitis by 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats prevented histological changes induced in the colon and the associated rise in inflammatory mediators. This study was therefore conducted to investigate whether ectoine (1) and its 5α-hydroxy derivative (2) would also be effective in treating an already established condition. Two days after inducing colitis in rats by instilling TNBS/alcohol in the colon, animals were treated orally once daily for 1 week with either 1 or 2 (50, 100, 300 mg/kg). Twenty-four hours after the last drug administration rats were sacrificed. Ulcerativ…

MaleColonInterleukin-1betaPharmaceutical SciencePharmacologyEctoineInflammatory bowel diseaseAnalytical Chemistrychemistry.chemical_compoundDrug DiscoverymedicineAnimalsHumansRats WistarColitisPeroxidasePharmacologyBacteriaMolecular StructurebiologyTumor Necrosis Factor-alphaChemistryOrganic ChemistryAmino Acids DiaminoGlutathioneColitisInflammatory Bowel DiseasesIntercellular Adhesion Molecule-1medicine.diseasebiology.organism_classificationGlutathioneRatsIntestinesSolutionsTrinitrobenzenesulfonic AcidComplementary and alternative medicineBiochemistryMyeloperoxidasebiology.proteinMolecular MedicineEgyptOsmoprotectantTumor necrosis factor alphaBacteriaJournal of Natural Products
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