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Pagina 1 a partire dal 274 risultati
Effect of N-tosyl-L-phenylalanylchloromethyl ketone on tumor necrosis factor-alpha -induced NF-kappaB activation and apoptosis in U937 cell line.
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To investigate the effect of N-tosyl-L-phenylalanylchloromethyl ketone (TPCK) on tumor necrosis factor-alpha-induced NF-kappaB activation and apoptosis in U937 cell line, changes and subcellular localization of NF-kappaB/p65 and IkappaB-alpha were observed by fluorescencemicroscopy and expression
The influence of ketone bodies and glucose on interferon, tumor necrosis factor production and NO release in bovine aorta endothelial cells.
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Bovine aorta endothelial cells (BAECs) were used to determine the effect of ketone bodies and glucose on in vitro interferon (IFN), tumor necrosis factor (TNF) and nitric oxide (NO) production. BAECs were incubated for 4 and 24h with the ketone bodies: 3.8mmol/l beta-hydroxybutyrate (BHB), 1mmol/l
A case of severe corrosive esophagitis, gastritis, and liver necrosis caused by ingestion of methyl ethyl ketone peroxide.
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The plastic hardener methyl ethyl ketone peroxide is unstable peroxide that releases free oxygen radicals. Ingestion of this compound induces widespread liver necrosis, severe metabolic acidosis, corrosive esophagitis and gastritis, that is often fatal. A 49-year-old man unintentionally ingested
Peripheral zonal hepatic necrosis caused by accidental ingestion of methyl ethyl ketone peroxide.
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Fatal massive peripheral zonal hepatic necrosis developed in a 47-year-old man who accidentally ingested a solution of methyl ethyl ketone peroxide (MEKP) in dimethyl phthalate. Such solutions contain about 10% active oxygen. The clinical course was characterized by temporary cardiac arrest,
Insulin-like growth factor I protects oligodendrocytes from tumor necrosis factor-alpha-induced injury.
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Tumor necrosis factor-alpha (TNF-alpha) has been causally implicated in several demyelinating disorders, including multiple sclerosis. Because insulin-like growth factor I (IGF-I) is a potent stimulator of myelination, we investigated whether it can protect oligodendrocytes and myelination from
Nitric-oxide-induced necrosis and apoptosis in PC12 cells mediated by mitochondria.
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Nitric oxide (NO) can trigger either necrotic or apoptotic cell death. We have used PC12 cells to investigate the extent to which NO-induced cell death is mediated by mitochondria. Addition of NO donors, 1 mM S-nitroso-N-acetyl-DL-penicillamine (SNAP) or 1 mM diethylenetriamine-NO adduct (NOC-18),
Photodynamic therapy in combination with talaporfin sodium induces mitochondrial apoptotic cell death accompanied with necrosis in glioma cells.
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Photodynamic therapy (PDT) induces selective cell death of neoplastic tissue and connecting vasculature by combining photosensitizers with light. Here we clarified the types of cell death induced by PDT in combination with the photosensitizer talaporfin sodium (mono-L-aspartyl chlorine e6, NPe6) in
Involvement of tumour necrosis factor in monocyte-mediated rapid killing of actinomycin D-pretreated WEHI 164 sarcoma cells.
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Human and murine monocyte-macrophages kill actinomycin D (ActD)-treated WEHI 164 sarcoma cells in a 6-hr 51Cr-release assay (drug-dependent cellular cytotoxicity, DDCC). In this study, we have investigated the cytotoxic activity of human recombinant tumour necrosis factor (hrTNF) against untreated
Pervanadate-induced nuclear factor-kappaB activation requires tyrosine phosphorylation and degradation of IkappaBalpha. Comparison with tumor necrosis factor-alpha.
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Tumor necrosis factor activates nuclear transcription factor kappaB (NF-kappaB) by inducing serine phosphorylation of the inhibitory subunit of NF-kappaB (IkappaBalpha), which leads to its ubiquitination and degradation. In contrast, pervanadate (PV) activates NF-kappaB and induces tyrosine
Irradiation up-regulates CD80 expression through induction of tumour necrosis factor-alpha and CD40 ligand expression on B lymphoma cells.
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Previously, we reported that 100 Gy X-ray irradiation followed by 24 hr incubation up-regulates CD80 expression in murine B lymphoma cells, A20-2J. In the present study, we analysed the underlying mechanisms of such up-regulation using A20-HL cells derived from A20-2J cells. Irradiation of A20-HL
The activity of cytosolic phospholipase A2 is required for the lysis of adenovirus-infected cells by tumor necrosis factor.
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Most cell types are resistant to apoptosis induced by tumor necrosis factor (TNF) unless the cells are treated with a sensitizing agent. Inhibitors of transcription or translation act as sensitizing agents, as do adenoviruses lacking one or more resistance genes. We have reported recently that the
Inhibitors of arachidonic acid metabolism potentiate tumour necrosis factor-alpha-induced apoptosis in HL-60 cells.
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We investigated whether and how could various modulators of arachidonic acid metabolism affect apoptosis induced by tumour necrosis factor-alpha (TNF-alpha) in human myeloid leukaemia HL-60 cells. These included arachinonyltrifluoromethyl ketone (AACOCF3; cytosolic phospholipase A2 inhibitor),
Tosylphenylalanine chloromethyl ketone inhibits TNF-alpha mRNA synthesis in the presence of activated NF-kappa B in RAW 264.7 macrophages.
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Serine proteinase inhibitors such as N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and N alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) were shown to inhibit production of tumour necrosis factor-alpha (TNF-alpha) in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. The proteinase
A1 functions at the mitochondria to delay endothelial apoptosis in response to tumor necrosis factor.
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Tumor necrosis factor (TNF) does not cause endothelial apoptosis unless the expression of cytoprotective genes is blocked. We have previously demonstrated that one of the TNF-inducible cytoprotective genes is the Bcl-2 family member, A1. A1 is induced by the action of the transcription factor,
Toxicological evaluation of z24, a novel indolin-2-ketone compound, in cultured human liver cells using toxicogenomic techniques.
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The current study was designed to investigate the toxicity of 3Z-3-[((1)H-pyrrol-2-yl)-methylidene]-1-(1-piperidinylmethyl)-1, 3-2H-indol-2-one (Z24), a novel synthetic indolin-2-ketone small molecule compound, using toxicogenomic techniques (complementary DNA [cDNA] microarray). Bioinformatic
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