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galactosamine/blødning
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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
[Activity of microsomal enzymes and lipid peroxidation in the liver in galactosamine injury].
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Galactosamine injury of rat liver brings about induction of microsomal oxidation enzymes after 24 hours. Such a conclusion may be arrived at on the basis of an analysis of variation in the activity of cytochrome P-450, cytochrome b5, and NADH ferricyanide reductase while comparing normal and
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
[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
Behaviour of 125I-fibrinogen and 131I-albumin in experimental galactosamine-induced hepatitis.
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The turnover of 125I-labelled fibrinogen and 131I-labelled albumin was studied in the course of galactosamine-induced hepatitis in rabbits. In addition to galactosamine, some animals were treated with epsilon-aminocaproic acid (EACA) to inhibit the activation of the fibrinolytic system. The infusion
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
Early growth response-1 contributes to galactosamine/lipopolysaccharide-induced acute liver injury in mice.
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Early growth response (Egr)-1 is a transcription factor that regulates genes involved in inflammation, innate and adaptive immunity, coagulation, and wound healing; however, little is known about the role of Egr-1 in acute liver injury. We tested the hypothesis that Egr-1 is involved in acute liver
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
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