d galactosamine/atrophy

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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%

[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

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

Cordyceps sinensis prevents apoptosis in mouse liver with D-galactosamine/lipopolysaccharide-induced fulminant hepatic failure.

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Cordyceps sinensis (C. sinensis) has long been considered to be an herbal medicine and has been used in the treatment of various inflammatory diseases. The present study examined the cytoprotective properties of C. sinensis on D(+)-galactosamine (GalN)/lipopolysaccharide (LPS)-induced fulminant

M1/M2-macrophage Polarization-based Hepatotoxicity in d-galactosamine-induced Acute Liver Injury in Rats.

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d-galactosamine (d-GalN) is a well-known hepatotoxic agent that causes liver injury. Conversely, hepatic macrophages play a crucial role in maintaining liver tissue integrity. Macrophage functions were investigated in hepatic lesions induced by a single intraperitoneal injection of d-GalN (800 mg/kg

Echinacoside ameliorates D-galactosamine plus lipopolysaccharide-induced acute liver injury in mice via inhibition of apoptosis and inflammation.

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OBJECTIVE This study aimed to investigate the protective effects of echinacoside, one of the phenylethanoids isolated from the stems of Cistanche salsa, a Chinese herbal medicine, on D-galactosamine (GalN) and lipopolysaccharide (LPS)-induced acute liver injury in mice. METHODS We administered GalN

The degradation of glycosaminoglycans by intestinal microflora deteriorates colitis in mice.

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The biosynthesis and modification of mucopolysaccharides and glycosaminoglycans (GAGs), secreted from gastrointestinal mucosal cells, are increased in colitis and influence the viability of the defense barrier. Therefore, to evaluate the role of GAG-degrading intestinal microflora during the

Protective effect of ultrasonication-processed ginseng berry extract on the D-galactosamine/lipopolysaccharide-induced liver injury model in rats.

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UNASSIGNED Acute hepatic failure is a life-threatening critical condition associated with rapid deterioration of liver function and liver transplantation. Several studies have shown that Panax ginseng Mayer has antidiabetic and hepatoprotective effects. However, the hepatoprotective effect of

Hepatosplanchnic haemodynamics and renal blood flow and function in rats with liver failure.

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BACKGROUND Massive liver necrosis, characteristic of acute liver failure, may affect hepatosplanchnic haemodynamics, and contribute to the alterations in renal haemodynamics and function. OBJECTIVE To investigate the relation between hepatosplanchnic haemodynamics, including portal systemic

Isolation and maintenance of monolayer hepatocytes from the livers of toxin-treated rats.

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Hepatocytes were isolated from male Sprague-Dawley rats 30 min after oral challenge with carbon tetrachloride (CCl4), or 1 hr after ip injection of D(+)-galactosamine (GAL). Cell preparations of comparable yield and initial viability were obtained from toxin-treated and respective control animals

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