nicotinamide/hypoxia

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Nicotinamide mononucleotide adenylyltransferase is a stress response protein regulated by the heat shock factor/hypoxia-inducible factor 1alpha pathway.

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Stress responses are cellular processes essential for maintenance of cellular integrity and defense against environmental and intracellular insults. Neurodegenerative conditions are linked with inadequate stress responses. Several stress-responsive genes encoding neuroprotective proteins have been

Nicotinamide pretreatment protects cardiomyocytes against hypoxia-induced cell death by improving mitochondrial stress.

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OBJECTIVE Nicotinamide plays a protective role in hypoxia-induced cardiomyocyte dysfunction. However, the underlying molecular mechanisms remain poorly understood. The purpose of this study was to investigate these and the effect of nicotinamide pretreatment on hypoxic

Reducing acute and chronic hypoxia in tumours by combining nicotinamide with carbogen breathing.

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The ability of nicotinamide and carbogen breathing to improve the radiation response of a C3H mammary carcinoma by reducing both acute and chronic hypoxia was investigated. Using a tumour growth delay assay the response of 200 mm3 foot tumours to local irradiation was found to be increased by either

[Effect of hypoxia on the concentration of nicotinamide coenzymes in the tissues of newborn rats].

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The content of nicotinamide coenzymes (NAD, NAD-H, NADP, NADP-H) was studied in the brain, heart and liver tissue of the newborn rats kept in hypoxic gaseous medium with a 4% oxygen content for 2 1/2 hours. There was a marked reduction of NAD content, an accumulation of NAD-H and a more than

Hypoxia inducible factor-1 alpha and vascular endothelial growth factor expression are associated with a poor prognosis in patients with nasopharyngeal carcinoma receiving radiotherapy with carbogen and nicotinamide.

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OBJECTIVE Hypoxia reduces tumour radiosensitivity and hypoxia inducible factor-1 alpha (HIF-1 alpha) plays an important role in this process. The aim of the study was to assess the prognostic impact of HIF-1 alpha and vascular endothelial growth factor (VEGF) in patients with nasopharyngeal

Protection effect of nicotinamide on cardiomyoblast hypoxia/re-oxygenation injury: study of cellular mitochondrial metabolism.

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Hypoxia/re-oxygenation (H/R) injury is an important cause of heart failure and results in a critical metabolism dysfunction. In this paper, the cytoprotective effect of the nicotinamide adenine dinucleotide (NAD) precursor nicotinamide was evaluated using an in vitro model of cardiac H/R injury.

Preclinical evidence of mitochondrial nicotinamide adenine dinucleotide as an effective alarm parameter under hypoxia.

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Early detection of tissue hypoxia in the intensive care unit is essential for effective treatment. Reduced nicotinamide adenine dinucleotide (NADH) has been suggested to be the most sensitive indicator of tissue oxygenation at the mitochondrial level. However, no experimental evidence comparing the

Nicotinamide Inhibits Glycolysis of HL-60 Cells by Modulating Sirtuin 1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Coactivator 1α (PGC-1α)/Hypoxia-Inducible Factor-2α (HIF2α) Signaling Pathway

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BACKGROUND Nicotinamide can affect differentiation and proliferation of leukemia cells. This research aimed to explore the regulatory effect of nicotinamide on glycolysis metabolism of leukemia cells and to clarify the associated mechanisms. MATERIAL AND METHODS HL-60 cells were treated with

Promotion of anoxia-reoxygenation-induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase-activated MAPK signaling in human umbilical vein endothelial cells.

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Previous studies have demonstrated that nicotinamide phosphoribosyltransferase (NAMPT) promoted inflammation and permeability of vascular endothelial cells following cardiopulmonary bypass (CPB). In addition, mitogen-activated protein kinase (MAPK) signaling was activated and contributed to these

Protective effect of nicotinamide on neuronal cells under oxygen and glucose deprivation and hypoxia/reoxygenation.

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Nicotinamide (vitamin B(3)) reduces the infarct volume following focal cerebral ischemia in rats; however, its mechanism of action has not been reported. After cerebral ischemia and/or reperfusion, reactive oxygen species (ROS) and reactive nitrogen species may be generated by inflammatory cells

[Influence of isolanide and trasicor on the content of nicotinamide coenzymes in the myocardium of growing rats in hemic hypoxia].

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Hemic hypoxia was produced in 7,30-day and 3--5-month old (adult) rats through introduction of sodium nitrite (100 mg/kg) with subsequent determination of the nicotinamide co-enzymes content in the myocardium. The effect of combined and separate application of the cardiac glycoside isolanide and

Nicotinamide and pentoxifylline increase human leucocyte filterability: a possible mechanism for reduction of acute hypoxia.

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Transient plugging of microcapillaries by leucocytes is a possible reason for the occurrence of acute hypoxia in tumours. We compared the abilities of nicotinamide at 1000 micrograms ml-1 and 150 micrograms ml-1 and pentoxifylline at 300 micrograms ml-1 to increase the filterability of normal and

Modulation of hypoxia in murine liver metastases of colon carcinoma by nicotinamide and carbogen.

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There is increasing evidence that modulation of tumor hypoxia may improve therapy outcome. However, most preclinical data are derived from subcutaneous rather than orthotopic tumor models. We investigated the effect of the hypoxia-modulating agents nicotinamide and carbogen on tumor hypoxia, tumor

Nicotinamide exacerbates hypoxemia in ventilator-induced lung injury independent of neutrophil infiltration.

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BACKGROUND Ventilator-induced lung injury is a form of acute lung injury that develops in critically ill patients on mechanical ventilation and has a high degree of mortality. Nicotinamide phosphoribosyltransferase is an enzyme that is highly upregulated in ventilator-induced lung injury and

Oversecretion and Overexpression of Nicotinamide Phosphoribosyltransferase/Pre-B Colony-Enhancing Factor/Visfatin in Inflammatory Bowel Disease Reflects the Disease Activity, Severity of Inflammatory Response and Hypoxia.

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Nicotinamide phosphoribosyltransferase's (Nampt) association with inflammatory bowel disease (IBD) is unclear. The study was aimed at unraveling Nampt's clinical and diagnostic relevance. The serum concentration (Luminex-xMAP® technology) was measured in 113 patients with Crohn's disease (CD), 127

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