galactosamine/atrofie

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[Establishment of a rat model of acute liver failure by a modified 90% bloodless hepatectomy and by D-galactosamine and lipopolysaccharide injection].

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OBJECTIVE To compare the effects of different approaches to establishing rat models of acute liver failure (ALF). METHODS Sixty-eight Sprague-Dawley rats were randomly divided into 3 groups for establishing ALF models using 3 different approaches, namely conventional hepatectomy for resecting 90%

Appearance of PNA-binding cells within the outer nuclear layer coinciding with photoreceptor degeneration in rd mice.

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Peanut agglutinin (PNA), a lectin with affinity for galactose-galactosamine disaccharides, has been employed to monitor alterations in carbohydrate expression in retinal degenerative (rd) mice. Mice homozygous for the rd gene exhibit a rapid loss of rod photoreceptor cells in the first postnatal

Cytoprotective effect of 16, 16' dimethyl prostaglandin E2 and some drugs on an acute galactosamine induced liver damage in rat.

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Present experiment was aimed to study whether 16, 16' dimethylprostaglandin E2 (dmPGE2), Hepatofalk (HF), or Orotofalk (OF) may prevent an acute liver damage induced in rats with D-galactosamine (GalN). Fifty male rats were divided into 5 groups: 1. controls, 2. rats receiving GalN 750 mg/kg b. w.

Stage-specific binding of peanut agglutinin to aggregates of degenerating photoreceptor cells in the rd mouse retina.

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Peanut agglutinin, a lectin with high binding affinity for galactose-galactosamine disaccharide, was used to monitor changes in the photoreceptor cell layer of mice with inherited retinal degeneration. Mice homozygous for the retinal degeneration (rd) gene exhibit a rapid loss of rod photoreceptor

[Protective effects of DBcAMP on acute liver failure induced by D-galactosamine in rats].

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We studied protective effects of Dibutyryl cyclic AMP (DBcAMP) which is a permeable form of cyclic AMP (cAMP), the intracellular second messenger, on D-galactosamine (D-Gal, 1.5g/kg i.p.) induced acute liver failure. Experimental animals were divided into four groups: Group I; DBcAMP was

Modification of D-galactosamine-induced liver damage in rats by intravenous injection of newly isolated intact splenic cells.

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In rats of an inbred F344/DuCrj line, simultaneous injection of newly isolated intact splenic cells (derived from normal rats of the same strain) markedly modified and reduced the liver damage induced by treatment with D-galactosamine. When rats treated with D-galactosamine plus newly isolated

Prevention of lethal hepatic injury in Long-Evans Cinnamon (LEC) rats by D-galactosamine hydrochloride.

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Repeated injections of D-galactosamine hydrochloride (GalN) increase the survival rate of Long-Evans Cinnamon (LEC) rats, an animal model of Wilson's disease. The aim of the present study was to investigate the mechanism of GalN for prevention of spontaneous lethal hepatic injury in LEC rats. Male

NO contribution to lipopolysaccharide-induced hepatic damage in galactosamine-sensitized mice.

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To investigate the role of nitric oxide (NO) in hepatitis-induced endotoxemia, we injected mice intraperitoneally with 250 mg/kg galactosamine (GalN) and 1 mg/kg lipopolysaccharide (LPS) separately and in combination. NO synthesis increased in a dose-dependent manner with LPS. NO generation at 5 hr

Biochemical markers in carbon-tetrachloride-and galactosamine-induced acute liver injuries: the effects of dihydroquinoline-type antioxidants.

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The pharmacological action and possible therapeutic uses of some recently developed synthetic, non-toxic dihydroquinoline-type antioxidants were studied. The effect of the lipid-soluble 6,6-methylene-bis (2,2,4-trimethyl-1,2-dihydroquinoline) (n = 1, 2 or 3) (MTDQ) on carbon-tetrachloride-induced

Apoptosis of murine hepatocytes induced by high doses of galactosamine.

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Apoptosis induced by high doses of Galactosamine (GalN) was investigated in mice hepatocytes in vivo. In mice intraperitoneally (i.p.) treated with GalN 3 g/kg, the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells were first observed at 6 hr

Pathological study of chronic D-galactosamine induced hepatitis in mice by administration of adjuvants - an animal model of the chronic active hepatitis.

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An animal model for human chronic active hepatitis was created in inbred C-57 Black mice using prolonged (13 weeks) administration of D-Galactosamine (GalN) and adjuvants. Intraperitoneal injections of GalN (1,500 mg/kg) were repeated once a week. Simultaneously, Freund's complete adjuvant (FCA) was

[Prophylactic and therapeutic effect of oxymatrine on D-galactosamine-induced rat liver fibrosis].

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OBJECTIVE To investigate the prophylactic and therapeutic effect of oxymatrine on experimental liver fibrosis and to reveal its mechanism. METHODS By establishing D-galactosamine-induced rat liver fibrosis model, we observed the effect of oxymatrine on serum and tissue biochemical indexes, content

Effect of silibinin and vitamin E on the ASK1-p38 MAPK pathway in D-galactosamine/lipopolysaccharide induced hepatotoxicity.

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Apoptosis signal-regulating kinase 1 (ASK1), a redox-sensor mitogen-activated protein kinase kinase kinase (MAPKKK) that activates p38 MAPK pathways in oxidative stress-induced hepatotoxicity in D-galactosamine/lipopolysaccharide (D-GalN/LPS) model, is a key central pathway in which specific

Protoberberine alkaloids from Enantia chlorantha therapy of allyl-alcohol- and D-galactosamine-traumatized rats.

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The short-term effect of the hepatotoxins allyl alcohol (AA) and D-galactosamine (GalN) was investigated in adult female rats. In addition, the curative effect of Hepasor, protoberberine extract from Enantia chlorantha was examined 3 days following traumatization. There was a significant increase in

Antinecrotic effect of 3-palmitoyl-(+)-catechin against liver damage induced by galactosamine or ethanol in the rat.

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The antinecrotic potential of a new drug, 3-palmitoyl-(+)-catechin (PC), which is a derivative of (+)-cyanidanol-3, was studied in two different experimental models of necrosis of the liver in the rat: acute hepatitis induced by galactosamine and liver damage induced by a combination of chronic

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