d galactosamine/hemorrhage

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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%

A role of cell apoptosis in lipopolysaccharide (LPS)-induced nonlethal liver injury in D-galactosamine (D-GalN)-sensitized rats.

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Lipopolysaccharide (LPS) is implicated in the pathology of acute liver injury and can induce lethal liver failure when simultaneously administered with D-galactosamine (D-GalN). At the present time, nonlethal liver failure, the liver injury of clinical implication, is incompletely understood

Sphingosine kinase 1 inhibition improves lipopolysaccharide/D-galactosamine-induced acute liver failure by inhibiting mitogen-activated protein kinases pathway.

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BACKGROUND Sphingosine kinase 1 (SphK1)/sphingosine-1-phosphate (S1P)/sphingosine-1-phosphate receptors (S1PRs) signaling plays a key role in inflammatory responses. Lei et al. showed that SphK1 inhibition presented a hepatoprotective effect on acute liver damage via decreasing hepatic high-mobility

Recql5 protects against lipopolysaccharide/D-galactosamine-induced liver injury in mice.

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OBJECTIVE To investigate the effects of Recql5 deficiency on liver injury induced by lipopolysaccharide/D-galactosamine (LPS/D-Gal). METHODS Liver injury was induced in wild type (WT) or Recql5-deficient mice using LPS/D-Gal, and assessed by histological, serum transaminases, and mortality analyses.

Urinary trypsin inhibitor protects against liver injury and coagulation pathway dysregulation induced by lipopolysaccharide/D-galactosamine in mice.

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Urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used for patients with inflammatory disorders including disseminated intravascular coagulation, shock, and pancreatitis in Japan. Our recent studies using UTI-null (-/-) mice have shown that UTI protects against systemic

Pim-3 protects against hepatic failure in D-galactosamine (D-GalN)-sensitized rats.

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BACKGROUND Fulminant hepatic failure (FHF) has a high mortality resulted from massive hepatic apoptosis and haemorrhage necrosis; it is required to develop a valid therapy directed towards hepatocyte protection and regeneration. Pim-3, a hepatic growth stimulator, belongs to the serine/threonine

[CD38 protein reduces LPS/D-galactosamine-induced acute damage of liver tissues via down-regulating inflammatory cytokine expressions].

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OBJECTIVE To investigate the role of CD38 in lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute hepatic injury in mice and explore the potential mechanism. METHODS A mouse model of acute hepatic injury was induced by an intraperitoneal injection (i.p.) of D-GalN and LPS. C57BL/6

Deficiency of interleukin-19 exacerbates lipopolysaccharide/D-galactosamine-induced acute liver failure

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Interleukin (IL)-19 is a cytokine clustered in the IL-20 cytokine superfamily with both anti-inflammatory and pro-inflammatory aspects depending on the etiology of inflammatory disease. The function of IL-19 has been evaluated in cutaneous and inflammatory bowel diseases, but has not been studied in

Insulin-like growth factor-I prevents lethal acute liver failure induced by D-galactosamine and lipopolysaccharide in rats.

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The aim of this study was to evaluate the effect of insulin-like growth factor-I (IGF-I) on lethality and liver function in experimental acute liver failure. Intravenous co-administration of D-galactosamine (GalN) and lipopolysaccharide (LPS) to rats induced high mortality and marked increases in

Ultrastructural study of development of hepatic necrosis induced by TNF-alpha and D-galactosamine.

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Recent studies have suggested an association between tumor necrosis factor-alpha (TNF-alpha) and the development and progression of acute liver failure. To investigate the role of TNF-alpha in the mechanism of massive hepatic necrosis, we studied a mouse model of TNF-alpha and D-galactosamine (GalN)

Possible role of LECT2 as an intrinsic regulatory factor in SEA-induced toxicity in d-galactosamine-sensitized mice.

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To elucidate whether leukocyte cell-derived chemotaxin 2 (LECT2) controls the progression of staphylococcal enterotoxin A (SEA)-induced toxicity, we examined the role of LECT2 in a mouse model. Almost all the C57BL/6J (B6) mice survived for 72 h after the injection of 0.1 μg of SEA and 20 mg of

A murine model of NKT cell-mediated liver injury induced by alpha-galactosylceramide/d-galactosamine.

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Natural killer-T (NKT) cells are rich in the liver. However, their involvement in liver injury is not fully understood. We developed here a new murine model of NKT-cell-activation-associated liver injury, and investigated a role of tumor necrosis factor alpha (TNF-alpha) and Fas in pathogenesis. We

Hepatoprotective and Antioxidant Capacity of Mallotus repandus Ethyl Acetate Stem Extract against d-Galactosamine-Induced Hepatotoxicity in Rats.

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Mallotus repandus (M. repandus) is traditionally used to treat muscle pain, itching, fever, rheumatic arthritis, and a variety of liver disorders. The aim of the present work was to evaluate the hepatoprotective activity and the antioxidant potential of the ethyl acetate stem extract

PEGylated lactoferrin enhances its hepatoprotective effects on acute liver injury induced by D-galactosamine and lipopolysaccharide in rats.

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Polyethylene glycol (PEG) is attached to proteins in order to increase their half-life in circulation and reduce their immunogenicity in vivo. The present study was conducted to examine whether two different sizes of PEGylated bovine lactoferrin (40k- and 20k-PEG-bLf) would enhance the protective

Protective effect of p-methoxyl-diphenyl diselenide in lethal acute liver failure induced by lipopolysaccharide and D-galactosamine in mice.

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Organoselenium compounds display important antioxidant activity and many biological activities interesting from pharmacological point of view. The aim of this study was to evaluate the hepatoprotective effect of p-methoxyl-diphenyl diselenide, a disubstituted diaryl diselenide, on acute liver injury

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