Search results for "tumor necrosis factor alpha"

showing 10 items of 479 documents

The carbon monoxide-releasing molecule CORM-2 inhibits the inflammatory response induced by cytokines in Caco-2 cells

2007

Background and purpose: Recent evidence indicates that carbon monoxide-releasing molecules (CO-RMs) exhibit potential anti-inflammatory properties. In the present study, we have investigated whether tricarbonyl dichloro ruthenium(II) dimer (CORM-2) can control the inflammatory response induced by cytokines in a human colonic epithelial cell line, Caco-2. Experimental approach: Caco-2 cells were preincubated with CORM-2 for 30 minutes and then stimulated with interleukin (IL)-1β, tumor necrosis factor-α and interferon-γ for different times. Gene expression was analyzed by real-time PCR. Protein expression was investigated by Western blot and ELISA. Transcription factor activation was determi…

PharmacologySmall interfering RNACytokinep38 mitogen-activated protein kinasesEnhancer bindingmedicine.medical_treatmentGene expressionmedicineTumor necrosis factor alphaBiologyNFKB1Protein kinase AMolecular biologyBritish Journal of Pharmacology
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Reduction of tumor necrosis factor-alpha (TNF-α) related nuclear factor-kappaB (NF-κB) translocation but not inhibitor kappa-B (Iκ-B)-degradation by …

2002

Degradation of inhibitor kappa-B (Ikappa-B) followed by translocation of nuclear factor-kappaB (NF-kappaB) into the nucleus and activation of gene expression is essential in tumor necrosis factor-alpha (TNF-alpha)-signaling. In order to analyze the role of Rho proteins in TNF-alpha-induced NF-kappaB-activation in human umbilical cord vein endothelial cells (HUVEC) we used Clostridium difficile toxin B-10463 (TcdB-10463) which inactivates RhoA/Rac1/Cdc42 by glucosylation and Clostridium botulinum C3-toxin which inhibits RhoA/B/C by ADP-ribosylation. Exposure of HUVEC to 10 ng/mL TcdB-10463 or 2.5 microg/mL C3-toxin inhibited TNF-alpha (100 ng/mL)-induced expression of a NF-kappaB-dependent r…

PharmacologyTRAF2RHOATumor Necrosis Factor-alphaNF-kappa BClostridium difficile toxin ABiological TransportRAC1Chromosomal translocationDNABiologyBiochemistryMolecular biologyRho kinase inhibitorbiology.proteinHumansI-kappa B ProteinsTumor necrosis factor alphaEndothelium VascularInterleukin 8rhoA GTP-Binding ProteinCells CulturedBiochemical Pharmacology
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Increased Percentages of Tumor Necrosis Factor-α+/Interferon-T+Lymphocytes and Calprotectin+/Tumor Necrosis Factor-A+ Monocytes in Patients with Acut…

2012

In vivo exposure to microorganisms resident in the oral cavity is considered as a possible cause of Kawasaki disease (KD), and some epitopes derived from streptococci display homology with Factor H of Complement. Additionally, calprotectin, a major calcium binding protein released by neutrophils and activated monocytes, could be directly involved in endothelial damage occurring in KD. The aim of our study is to evaluate the percentages of IFN-γ+ and/or TNF-α+ lymphocytes and double positive calprotectin/TNF-α monocytes (CD14+) after in vitro stimulation with streptococcal- and/or Factor H-derived peptides, in patients with acute KD. Peripheral Blood Mononuclear Cells (PBMCs) obtained from …

Pharmacologybusiness.industryImmunologymedicine.diseaseEpitopeInterferonIn vivoImmunologymedicineImmunology and AllergyIn patientKawasaki diseaseTumor necrosis factor alphaCalprotectinbusinessTumor necrosis factor αmedicine.drugInternational Journal of Immunopathology and Pharmacology
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Erythromycin exertsin vivoanti-inflammatory activity downregulating cell adhesion molecule expression

2005

1. Macrolides have long been used as anti-bacterial agents; however, there is some evidence that may exert anti-inflammatory activity. Therefore, erythromycin was used to characterize the mechanisms involved in their in vivo anti-inflammatory activity. 2. Erythromycin pretreatment (30 mg kg(-1) day(-1) for 1 week) reduced the lipopolysaccharide (LPS; intratracheal, 0.4 mg kg(-1))-induced increase in neutrophil count and elastase activity in the bronchoalveolar lavage fluid (BALF) and lung tissue myeloperoxidase activity, but failed to decrease tumor necrosis factor-alpha and macrophage-inflammatory protein-2 augmented levels in BALF. Erythromycin pretreatment also prevented lung P-selectin,…

Pharmacologymedicine.diagnostic_testLipopolysaccharideCell adhesion moleculeErythromycinPharmacologyBiologychemistry.chemical_compoundBronchoalveolar lavagechemistryIn vivoImmunologymedicineTumor necrosis factor alphaCell adhesionmedicine.drugAntibacterial agentBritish Journal of Pharmacology
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Antipsoriatic effects of avarol-3′-thiosalicylate are mediated by inhibition of TNF-αgeneration and NF-κB activation in mouse skin

2007

Background and purpose: Avarol is a marine sesquiterpenoid hydroquinone with anti-inflammatory and antipsoriatic properties. The aim of this study was to evaluate the in vitro and in vivo pharmacological behaviour of the derivative avarol-3′-thiosalicylate (TA) on some inflammatory parameters related to the pathogenesis of psoriasis. Experimental approach: Human neutrophils and monocytes as well as the human keratinocyte cell line HaCaT were used to study the effect of TA on oxidative stress, the arachidonic acid pathway, tumour necrosis factor-α (TNF-α) release and nuclear factor-κB (NF-κB) activation. All these parameters were also determined in vivo using the zymosan induced mouse air po…

Pharmacologymedicine.medical_specialtyLeukotriene B4ZymosanPharmacologyBiologyNFKB1HaCaTchemistry.chemical_compoundmedicine.anatomical_structureEndocrinologyEicosanoidchemistryIn vivoInternal medicinemedicineTumor necrosis factor alphaKeratinocyteBritish Journal of Pharmacology
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Cacospongionolide B suppresses the expression of inflammatory enzymes and tumour necrosis factor-αby inhibiting nuclear factor-κB activation

2003

The marine product cacospongionolide B, a sesterterpene isolated from the Mediterranean sponge Fasciospongia cavernosa, is an inhibitor of secretory phospholipase A2 with anti-inflammatory properties. In this work, we have studied the mechanism of action of this compound in the inflammatory response induced by zymosan in primary cells and in the mouse air pouch. In mouse peritoneal macrophages, cacospongionolide B was able to downregulate the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), resulting in decreased production of NO and prostaglandin E2 (PGE2). This compound also reduced tumour necrosis factor-α (TNF-α) mRNA expression and TNF-α levels. Cacosp…

Pharmacologymedicine.medical_specialtyNecrosisbiologyZymosanNFKB1Molecular biologyNitric oxide synthasechemistry.chemical_compoundEndocrinologyMechanism of actionchemistryInternal medicinemedicinebiology.proteinTumor necrosis factor alphamedicine.symptomProstaglandin E2Transcription factormedicine.drugBritish Journal of Pharmacology
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Pentoxifylline in liver ischemia and reperfusion.

2013

Pentoxifylline is a methylxanthine compound which was first filed in 1973 and registered in 1974 in the United States by Sanofi-Aventis Deustchland Gmbh for the treatment of intermittent claudication for chronic occlusive arterial disease. This methylxanthine was later discovered to be a phosphodiesterase inhibitor. Furthermore, its hemorheological properties and its function as an inhibitor of inflammatory cytokines, like TNF- α, allowed researchers to study its effects in organ ischemia and reperfusion and transplantation. Although this drug has demonstrated beneficial effects, the mechanisms by which Pentoxifylline exerts a protective effect are not fully understood. This paper focuses o…

Phosphodiesterase InhibitorsIschemiaApoptosisPharmacologyPentoxifyllineProinflammatory cytokineIschemiamedicineAnimalsHumansPhosphodiesterase inhibitorPentoxifyllinebusiness.industryTumor Necrosis Factor-alphaLiver Diseasesmedicine.diseaseIntermittent claudicationLiver TransplantationTransplantationLiverAnesthesiaReperfusion InjurySurgeryTumor necrosis factor alphamedicine.symptombusinessReperfusion injurymedicine.drugJournal of investigative surgery : the official journal of the Academy of Surgical Research
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Antisense Phosphorothioate Oligonucleotides to the p65 Subunit of NF-κB Abrogate Fulminant Septic Shock Induced byS. typhimuriumin Mice

2001

The aim of this study was to characterize the functional relevance of the transcription factor NF-κB in the pathogenesis of septic shock. BALB/c mice were infected with two wild-type (WT 1, WT 2) strains of S. typhimurium that induce NF-κB or an escape variant that lacks this ability (P21) at a dose of 1 × 109/animal, respectively. Furthermore, wild-type infected mice were treated with antisense oligonucleotides directed against NF-κB 24 h before and 3 or 6 h after infection, while mismatched oligonucleotides were used as controls. Subsequently, the clinical course, histological and immunological alterations were monitored. Infection with WT 1 and WT 2 strains led to lethal septic shock wit…

Phosphorothioate OligonucleotidesNecrosisSeptic shockFulminantImmunologyInterleukinGeneral MedicineBiologymedicine.diseaseVirologyMolecular biologyPathogenesisInterferonmedicineTumor necrosis factor alphamedicine.symptommedicine.drugScandinavian Journal of Immunology
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Interleukin 23p19 inhibitors in chronic plaque psoriasis with focus on mirikizumab: A narrative review.

2020

Psoriasis, a T-cell mediated chronic dermatosis, has a complex etiopathogenesis. There has been extensive research into the aberrant immune response, which leads to the formation of clinical lesions, and the need for developing better and safer drugs has been unrelenting. The past two decades of research has opened up new areas of the immune pathway that can be targeted in order to control the disease. Therefore, we have seen the emergence of biologics which either target T-cell receptors or inhibit Tumor Necrosis Factor-alpha (TNF-α) or inhibit interleukins (IL) like IL-12, IL-17, IL-17 receptor, and more recently IL-23. Drugs specifically targeting the p19 subunit of IL-23 have shown prom…

Plaque psoriasisCell signalingbusiness.industryInterleukinDermatologyGeneral MedicineDiseasemedicine.diseaseAntibodies Monoclonal HumanizedInterleukin-23030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineImmune system030220 oncology & carcinogenesisPsoriasisImmunologymedicineHumansPsoriasisTh17 CellsTumor necrosis factor alphaReceptorbusinessDermatologic therapyREFERENCES
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Regulation of tumour cell sensitivity to TNF-induced oxidative stress and cytotoxicity: Role of glutathione

1998

Glutathione (GSH) and the rate of cellular proliferation determine tumour cell sensitivity to tumour necrosis factor (TNF). Buthionine sulphoximine (BSO), a selective inhibitor of GSH synthesis, inhibits tumour growth and increases recombinant human TNF (rhTNF)-alpha cytoxicity in vitro. Administration of sublethal doses of rhTNF-alpha to Ehrlich ascites-tumour (EAT)-bearing mice induces oxidative stress (as measured by increases in intracellular peroxide levels, O2.- generation and mitochondrial GSSG). ATP-induced selective GSH depletion, when combined with rhTNF-alpha administration, affords a 61% inhibition of tumour growth and results in a significant extent of host survival. Administra…

Programmed cell deathCell SurvivalClinical BiochemistryMitochondrionPharmacologyBiologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesmedicineAnimalsHumansCarcinoma Ehrlich TumorGlutathione DisulfideTumor Necrosis Factor-alphaGeneral MedicineGlutathioneGlutathioneRecombinant ProteinsOxidative StresschemistryBiochemistryCancer cellMolecular MedicineGlutathione disulfideTumor necrosis factor alphaOxidative stressIntracellularBioFactors
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