galactosamine/necrotisch

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Late preventive effects of several anticalmodulin drugs on galactosamine-induced liver necrosis.

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Four anticalmodulin drugs: trifluoperazine (TFP), pimozide (PMZ), thioridazine (TDZ) and imipramine (IMP) (50 mg/kg, ip) were able to partially prevent Galactosamine (GAL) (600 mg/kg, ip) induced liver necrosis when given 6 h after the hepatotoxin. IMP was also effective 10 h after GAL. The

Prevention of galactosamine-induced liver cell necrosis by uridine.

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The administration of galactosamine to rats produces dose-dependent liver cell injury. A relatively low dose of galactosamine (200 mg/kg) causes a marked fall in UTP with an accompanying inhibition of RNA and protein synthesis. Uridine will reverse the UTP deficiency and the inhibition of RNA and

Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin-1 or tumour necrosis factor by D-galactosamine.

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1. An injection of D-galactosamine (GalN) into mice together with a lipopolysaccharide (LPS or endotoxin), interleukin-1 (IL-1) or tumour necrosis factor (TNF), sensitized the mice and induced fulminant hepatitis with severe congestion resulting in rapid death. Since LPS and these cytokines induce

Late preventive effects on dimethylnitrosamine, thioacetamide or galactosamine-induced liver necrosis of the inhibitor of proteases, phenylmethylsulfonyl fluoride.

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Phenylmethylsulfonyl fluoride (PMSF) administration to rats, was effective in partially preventing liver necrosis induced by thioacetamide, dimethylnitrosamine or galactosamine, when given 6 hr after the hepatotoxins. In the case of galactosamine but not of the other necrogenic chemicals, protection

Evaluation of oxidative stress during apoptosis and necrosis caused by D-galactosamine in rat liver.

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Eighteen and twenty-four hours after intraperitoneal administration of D-galactosamine (1g/kg body weight) to rats, the activity of caspase-3-like protease in the liver increased significantly compared with that in the control group given saline. Histological examinations including the in situ

Caspase activation during hepatocyte apoptosis induced by tumor necrosis factor-alpha in galactosamine-sensitized mice.

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OBJECTIVE To clarify the mechanism of hepatocyte apoptosis induced by tumor necrosis factor-alpha (TNF-alpha), caspase cascade and ceramide formation were investigated in the liver of D-galactosamine (GalN)-sensitized mice treated with TNF-alpha. METHODS Seven-week-old male BALB/c mice were

Protective effects of E3330, a novel quinone derivative, on galactosamine/tumor necrosis factor-alpha-induced hepatitis in mice.

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Oral pretreatment with E3330, a novel quinone derivative, attenuated liver injury induced with tumor necrosis factor-alpha in galactosamine-sensitized mice. Tumor necrosis factor-alpha is known to induce inflammatory mediators such as leukotrienes and prostanoids. An in vitro study showed that E3330

Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis.

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Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Activation of nuclear factor kappa B (NF-kappa B) and expression of apoptotic Bcl-2 family members

Alterations in the indexes of apoptosis and necrosis induced by galactosamine in the liver of Wistar rats treated with fructose-1,6-bisphosphate.

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Galactosamine (GalN) is a hepatotoxic agent, which under determined situations provokes metabolic and energetic depletion as well as alterations in permeability, leading to cellular death. At the same time, it is known that fructose-1,6-bisphosphate (FBP) helps maintain cell energy levels and

Tumour necrosis factor-alpha and nitric oxide mediate apoptosis by D-galactosamine in a primary culture of rat hepatocytes: exacerbation of cell death by cocultured Kupffer cells.

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BACKGROUND Prostaglandin E1 (PGE1) reduces cell death in experimental and clinical liver dysfunction. OBJECTIVE Whether PGE1 protects against D-galactosamine (D-GalN)-associated hepatocyte cell death by the regulation of tumour necrosis factor-alpha (TNF-alpha) and/or nitric oxide (NO) in

Role of FAN in tumor necrosis factor-alpha and lipopolysaccharide-induced interleukin-6 secretion and lethality in D-galactosamine-sensitized mice.

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Tumor necrosis factor (TNF) alpha-induced neutral sphingomyelinase-mediated generation of ceramide, a bioactive lipid molecule, is transduced by the adaptor protein FAN, which binds to the intracellular region of the CD120a TNFalpha receptor. FAN-deficient mice do not exhibit any gross abnormality.

Enhancement by galactosamine of lipopolysaccharide(LPS)-induced tumour necrosis factor production and lethality: its suppression by LPS pretreatment.

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1. D-Galactosamine (GalN) depletes UTP primarily in the liver, resulting in decreased RNA synthesis in hepatocytes. Co-injection of GalN and lipopolysaccharide (LPS) into mice produces fulminant hepatitis with severe hepatic congestion, resulting in rapid death. Although the underlying mechanism is

Interleukin-10 inhibits hepatic injury and tumor necrosis factor-alpha and interferon-gamma mRNA expression induced by staphylococcal enterotoxin B or lipopolysaccharide in galactosamine-sensitized mice.

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OBJECTIVE Proinflammatory cytokines including tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) play a critical role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) or staphylococcal enterotoxin B (SEB) in D-galactosamine (GalN)-sensitized mice. The aim

Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism.

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OBJECTIVE The aim was to determine the action mode of cornel iridoid glycoside (CIG) from Fructus corni on hepatoprotective activities, the effects of CIG on human hepatocyte cell line (L02) injured by D-galactosamine (GalN) and tumor necrosis factor-α (TNF-α) were examined. METHODS The percentage

Bilirubin release induced by tumor necrosis factor in combination with galactosamine is toxic to mice.

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Application of tumor necrosis factor (TNF) in combination with galactosamine (GalN) in mice causes severe apoptosis of hepatocytes, resulting in complete destruction of the liver. Administration of high levels of unconjugated bilirubin and abnormally high production of unconjugated bilirubin have

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