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Effects of isothiocyanates on tumor necrosis factor-alpha production by J774A.1 (BALB/c macrophage) cells.

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The effects of isothiocyanates (ITCs) on tumor necrosis factor-alpha (TNF-alpha) production by the J774A.1 mouse macrophage cell line stimulated with lipopolysaccharide (LPS) were examined. Some individual ITCs examined showed a priming effect, which was expressed as pre-activation, but also

Allyl isothiocyanate (AITC) and phenyl isothiocyanate (PITC) inhibit tumour-specific angiogenesis by downregulating nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) production.

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Angiogenesis, a crucial step in the growth and metastasis of cancers, is initiated with vasodilation mediated by nitric oxide (NO). The pro-inflammatory cytokine, tumour necrosis factor-alpha (TNF-alpha), is a mediator of nitric oxide synthesis. We analyzed the effect of allyl isothiocyanate (AITC)

Acute cholecystitis and persistent liver necrosis in mice provoked by isothiocyanate.

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Two known cholangiotoxic agents, alpha-naphthylisothiocyanate (ANIT) and p-phenylenediisothiocyanate (PDT), were administered in single doses to mice to study their effects on the gallbladder. Both compounds caused maximal bile duct necrosis and periportal hepatocytic necrosis at 24 hours. In

Tumor necrosis factor-related apoptosis-inducing ligand promotes microvascular endothelial cell hyperpermeability through phosphatidylinositol 3-kinase pathway.

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BACKGROUND Microvascular hyperpermeability that occurs in hemorrhagic shock and burn trauma is regulated by the apoptotic signaling pathway. We hypothesized that tumor necrosis factor-α (TNF-α)-related apoptosis-inducing ligand (TRAIL) would promote hyperpermeability directly or by interacting with

Regulation of tumor necrosis factor-α-induced microvascular endothelial cell hyperpermeability by recombinant B-cell lymphoma-extra large.

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BACKGROUND Tumor necrosis factor-α (TNF-α), a cytotoxic cytokine, induces endothelial cell barrier dysfunction and microvascular hyperpermeability, leading to tissue edema, a hallmark of traumatic injuries. The objective of the present study was to determine whether B-cell lymphoma-extra large

Tumor necrosis factor-α-induced microvascular endothelial cell hyperpermeability: role of intrinsic apoptotic signaling.

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Tumor necrosis factor-α (TNF-α), a pro-apoptotic cytokine, is involved in vascular hyperpermeability, tissue edema, and inflammation. We hypothesized that TNF-α induces microvascular hyperpermeability through the mitochondria-mediated intrinsic apoptotic signaling pathway. Rat lung microvascular

Effect of tumor necrosis factor-alpha on the permeability of bovine brain microvessel endothelial cell monolayers.

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The administration of chemotherapy to patients with tumors of the central nervous system is often blocked by the blood-brain barrier. Tumor necrosis factor-alpha (TNF-alpha) is a cytokine that promotes vascular permeability in addition to its pro-inflammatory effects. However, no direct evidence

Mannitol protects hair cells against tumor necrosis factor α-induced loss.

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OBJECTIVE Mannitol has otoprotective effects against tumor necrosis factor (TNF) α-induced auditory hair cell (HC) loss. BACKGROUND Mannitol has been demonstrated to possess cytoprotective effects in several organ systems. Its protective effect on postischemic hearing loss has also been shown.

Tumour necrosis factor receptor II (p75) signalling is required for the migration of Langerhans' cells.

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Langerhans' cells (LC) represent the major antigen-presenting cells within the epidermis. Following exposure of the skin to antigen, LC take up antigen, migrate into draining lymph nodes (DLN) and present processed antigen to T lymphocytes, thereby initiating an immune response. The molecular

Cytokines and growth factors inhibit tumor necrosis factor alpha-induced up-regulation of fibronectin binding on bovine endometrial cells.

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OBJECTIVE To design a high-throughput cell assay to identify molecules modulating adhesion induced by tumor necrosis factor alpha (TNF-alpha) of endometrial cells to mesothelium. METHODS Prospective study. METHODS Biotech company. METHODS Bovine endometrial (BEND) and human mesothelial

Preclinical evaluation of 4-methylthiobutyl isothiocyanate on liver cancer and cancer stem cells with different p53 status.

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Isothiocyanates from plants of the order Brassicales are considered promising cancer chemotherapeutic phytochemicals. However, their selective cytotoxicity on liver cancer has been barely researched. Therefore, in the present study, we systematically studied the chemotherapeutic potency of

Reduction in neutrophil cell surface expression of tumor necrosis factor receptors but not Fas after transmigration: implications for the regulation of neutrophil apoptosis.

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OBJECTIVE To test the hypothesis that loss of polymorphonuclear neutrophil tumor necrosis factor alpha (TNF-alpha) receptors during transmigration renders the exudate neutrophil refractory to TNF-alpha-mediated stimulation of apoptosis; and to investigate the surface expression of Fas on both

Role of tumor necrosis factor-alpha and matrix metalloproteinase-9 in blood-brain barrier disruption after peripheral thermal injury in rats.

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OBJECTIVE A relationship has been found between peripheral thermal injury and cerebral complications leading to injury and death. In the present study, the authors examined whether tumor necrosis factor-alpha (TNF-alpha) and matrix metalloproteinase-9 (MMP-9) play a causative role in blood-brain

Inhibition of tumor necrosis factor alpha-induced vascular endothelial permeability by gadolinium chloride.

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Tumor necrosis factor-alpha (TNF alpha) is an important mediator of endotoxic and septic shock. We previously reported that the survival rate in a rat sepsis model was improved by the administration of gadolinium chloride (GdCl3), whereas the level of TNF alpha in the blood was not affected. In the

Induction of necrosis by zinc in prostate carcinoma cells and identification of proteins increased in association with this induction.

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Zinc exhibits inhibitory effects on apoptosis, and a deficiency in this metal generally causes this type of cell death to occur. In the present study, we found that exposure to zinc results in necrosis of prostate carcinoma cells. When zinc acetate was added to LNCaP or PC-3 cells in monolayer

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