niacinamide/necrosis

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Experimental study on inhibitory effect of niacinamide on tumor necrosis factor-alpha-induced matrix degradation of annulus fibrous tissue in vitro.

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The inhibitory effect of niacinamide on tumor necrosis factor-alpha (TNF-alpha) induced annulus fibrous (AF) degradation was assessed, and the mechanism of the inhibition was investigated. Chiba's intervertebral disc (IVD) culture model was established. Forty-eight IVDs from 12 adult Japanese white

Reduction of erythema in hairless guinea pigs after cutaneous sulfur mustard vapor exposure by pretreatment with niacinamide, promethazine and indomethacin.

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Erythema is the initial symptom that occurs after sulfur mustard (HD) cutaneous exposure. The time course of HD-induced erythema is similar to that observed after UV irradiation, which can be reduced by indomethacin. Sulfur mustard lethality is decreased by using promethazine, which is an

Cholera toxin induces tumor necrosis factor alpha production in human monocytes.

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Cholera toxin covalently ADP-ribosylates the a subunit of Gs proteins. The modified Gsalpha activates adenylate cyclase and leads to a dramatic increase in intracellular cAMP. The effect of cholera toxin on the production of tumor necrosis factor (TNF-alpha), a critical mediator of toxicity for a

Protective effects of niacinamide in staphylococcal enterotoxin-B-induced toxicity.

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Staphylococcal enterotoxins (SE) interact with major histocompatibility complex (MHC) class II cell-surface receptors, eliciting signal transduction in antigen-presenting cells (APC). Subsequent toxin-class II complex interaction with specific T-cell receptors induces T-cell activation. We

The protective effect of niacinamide on ischemia-reperfusion-induced liver injury.

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Reperfusion of ischemic liver results in the generation of oxygen radicals, nitric oxide (NO) and their reaction product peroxynitrite, all of which may cause strand breaks in DNA, which activate the nuclear enzyme poly(ADP ribose)synthase (PARS). This results in rapid depletion of intracellular

Inhibition of cytokine-induced MHC class II but not class I molecule expression on mouse islet cells by niacinamide and 3-aminobenzamide.

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Normal mouse islet cells express low levels of MHC class I molecules and undetectable or extremely low levels of MHC class II molecules. Class I expression was dose-dependently augmented by incubation with interferon-gamma (IFN-gamma) or tumor necrosis factor (TNF). Although neither IFN-gamma nor

Niacinamide abrogates the organ dysfunction and acute lung injury caused by endotoxin.

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Poly (ADP-ribose) synthabse (PARS) or polymerase (PARP) is a cytotoxic enzyme causing cellular damage. Niacinamide inhibits PARS or PARP. The present experiment tests the effects of niacinamide (NCA) on organ dysfunction and acute lung injury (ALI) following lipopolysaccharide (LPS). LPS was

Pathogenesis of 2,2'-dichlorodiethyl sulfide in hairless guinea pigs.

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Developing skin lesions on hairless guinea pigs due to 2,2'-dichlorodiethyl sulfide (sulfur mustard, HD) exposure were examined to determine the time course for the appearance of histopathologic markers in relationship to skin NAD+ and NADP+ content after HD exposure. Hairless guinea pig skin was

Downregulation of NF-kappaB activation in human keratinocytes by melanogenic inhibitors.

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BACKGROUND Exposure of skin cells, particularly keratinocytes to various nuclear factor-kappaB (NF-kappaB) activators (e.g. tumor necrosis factor-alpha, interleukin-1, lipopolysaccharides, and ultraviolet light) leads to phosphorylation and degradation of the inhibitory protein, IkappaB. Liberated

Pharmacological targeting of IDO-mediated tolerance for treating autoimmune disease.

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Cells at the maternal-fetal interface express indoleamine 2,3 dioxygenase (IDO) to consume all local tryptophan for the express purpose of starving adjacent maternal T cells of this most limiting and essential amino acid. This stops local T cell proliferation to ultimately result in the most

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