nicotinamide/edema

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Nicotinamide reduces acute cortical neuronal death and edema in the traumatically injured brain.

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Previous studies have shown that administration of nicotinamide (Vitamin B(3)) in animal models of traumatic brain injury (TBI) and ischemia significantly reduced the size of infarction or injury and improved functional recovery. The present study evaluated the ability of nicotinamide to provide

[Pathophysiological hypothesis regarding the role of nicotinamide in the genesis of niacin-induced macular edema].

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Mechanisms of transformation of nicotinamide mononucleotides to cerebral infarction hemorrhage based on MCAO model.

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The study aims at discussing the effect of nicotinamide mononucleotides on protecting hemorrhagic transformation of cerebral infarction in the middle cerebral artery occlusion (MCAO) model.Male mice aged 4-5 weeks and weighing about 22-35 g in Shanghai

Protective effects of poly (ADP-ribose) synthase inhibitors in zymosan-activated plasma induced paw edema.

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The aim of the present study was to investigate the role of poly (ADP-ribose) synthetase (PARS) in a model of acute local inflammation (zymosan-activated plasma (ZAP)-induced paw edema), in which the oxyradicals, nitric oxide and peroxynitrite, are known to play a crucial role. Injection of

Anti-Inflammation Effects and Potential Mechanism of Saikosaponins by Regulating Nicotinate and Nicotinamide Metabolism and Arachidonic Acid Metabolism.

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Inflammation is an important immune response; however, excessive inflammation causes severe tissue damages and secondary inflammatory injuries. The long-term and ongoing uses of routinely used drugs such as non-steroidal anti-inflammatory drugs (NSAIDS) are associated with serious adverse reactions,

Metabolic changes in nicotinamide adenine dinucleotide in response to anthrax toxin.

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Bacillus anthracis produces a toxin both in vitro and in vivo which, when injected intravenously into rats, brings about the death of the animals accompanied by gross pulmonary edema. Lung tissue removed prior to death showed, in vitro, a 30% reduction in overall oxidative metabolism (Q(o2)),

The effects of nicotinamide adenine dinucleotide on intracerebral hemorrhage-induced brain injury in mice.

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In the present study, we investigated whether the administration of nicotinamide adenine dinucleotide (NAD+) provides brain protection in a mouse model of intracerebral hemorrhage (ICH). Male CD-1 mice were divided into sham, ICH treated with vehicle and ICH treated with NAD+ (10 or 20 mg/kg,

β-Nicotinamide adenine dinucleotide attenuates lipopolysaccharide-induced inflammatory effects in a murine model of acute lung injury.

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) occur in approximately 200,000 patients per year. Studies indicate that lung endothelium plays a significant role in ALI. The authors' recent in vitro studies demonstrate a novel mechanism of β-nicotinamide adenine dinucleotide

A comparison of the effects of nicotinamide and progesterone on functional recovery of cognitive behavior following cortical contusion injury in the rat.

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The primary goal of this study was to compare clinically relevant doses of progesterone and nicotinamide within the same injury model. Progesterone has been shown to reduce edema and inflammation and improve functional outcomes following brain injury. Nicotinamide has also been shown to be an

Energy metabolism and cerebral blood flow during cytotoxic brain edema induced by 6-aminonicotinamide.

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We investigated the progression of cytotoxic brain edema induced by 6-aminonicotinamide (6-ANA), a potent antimetabolite of nicotinamide, by measuring the time courses of changes in brain tissue water state (with MRI), histology (with H&E staining), energy metabolism (with 31P-NMR), brain hemoglobin

Protection against LPS-induced pulmonary edema through the attenuation of protein tyrosine phosphatase-1B oxidation.

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One hallmark of acute lung injury is the disruption of the pulmonary endothelial barrier. Such disruption correlates with increased endothelial permeability, partly through the disruption of cell-cell contacts. Protein tyrosine phosphatases (PTPs) are known to affect the stability of both

Different Roles of N-Terminal and C-Terminal Domains in Calmodulin for Activation of Bacillus anthracis Edema Factor.

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Bacillus anthracis adenylyl cyclase toxin edema factor (EF) is one component of the anthrax toxin and is essential for establishing anthrax disease. EF activation by the eukaryotic Ca2+-sensor calmodulin (CaM) leads to massive cAMP production resulting in edema. cAMP also inhibits the nicotinamide

Rhubarb attenuates cerebral edema via inhibition of the extracellular signal-regulated kinase pathway following traumatic brain injury in rats.

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UNASSIGNED Rhubarb is a traditional Chinese medicine for treating traumatic brain injury (TBI). UNASSIGNED The purpose of this study is to elucidate the potential mechanism of rhubarb by suppressing extracellular signal-regulated kinase (ERK) to ameliorate brain edema. UNASSIGNED Sprague-Dawley rats

Brain edema and gliopathy induced by 6-aminonicotinamide intoxication in the central nervous system of rats.

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Brain edema was produced by 6-aminonicotinamide (6-AN) in the rat with accompanying metabolic disturbance due to the accumulation of an antimetabolite of nicotinamide in the CNS. Twenty-four hours after intraperitoneal administration of 6-AN, significant (P less than 0.01) increases of sodium and

[Sequential observations of brain edema with proton magnetic resonance imaging and spectroscopy].

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The purpose of this study was to assess the relationship between morphological and metabolic changes in brain edema using proton magnetic resonance systems. The serial changes during the first 24 hours in the cold-injury trauma rat brain model were investigated by proton magnetic resonance imaging

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