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galactosamine/hypoxia
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Intrahepatic microcirculatory disorder, parenchymal hypoxia and NOX4 upregulation result in zonal differences in hepatocyte apoptosis following lipopolysaccharide- and D-galactosamine-induced acute liver failure in rats.
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Although the mechanisms responsible for acute liver failure (ALF) have not yet been fully elucidated, studies have indicated that intrahepatic macrophage activation plays an important role in the pathogenesis of ALF through intrahepatic microcirculatory disorder and consequent parenchymal cell
Effects of nitroprusside as a nitric oxide donor on anoxia/reoxygenation and D-galactosamine hepatic injuries: a study in perfused hepatocytes.
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At present, the physiological role of NO. synthesis in the liver is ambiguous. Studies directed to reveal the role of NO. in relation to liver function were primarily initiated by an interest in the hepatic response to infections and the consequent modulation of liver function. The purpose of the
Effect of galactosamine-induced hepatitis on the aerobic and anaerobic metabolism of the rat exposed to high-altitude hypoxia.
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Galactosamine-induced hepatitis caused a marked increase in plasma lactate and pyruvate, but completely abolished the increase in ketone bodies in the rat exposed to an 8000 m simulated altitude. Plasma free fatty acid as the precursor of ketone bodies was higher in the galactosamine-treated rats
Brain edema in rabbits with galactosamine-induced fulminant hepatitis. Regional differences and effects on intracranial pressure.
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Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we
Metformin suppresses intrahepatic coagulation activation in mice with lipopolysaccharide/D‑galactosamine‑induced fulminant hepatitis.
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Metformin is a widely‑used antidiabetic drug with hypoglycemic activity and previously described anti‑inflammatory properties. Previous studies have demonstrated that metformin attenuates endotoxic hepatitis, however the mechanisms remain unclear. Inflammation and coagulation are closely associated
Hepatoprotective effects of salidroside on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in mice.
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OBJECTIVE
The aim was to investigate the protective effect of salidroside isolated from Rhodiola sachalinensis A. Bor. (Crassulaceae) on D-galactosamine/lipopolysaccharide-induced fulminant hepatic failure.
METHODS
Hepatotoxicity was induced by an intraperitoneal injection of D-galactosamine (700
The protective effects of total saponins from Ornithogalum saundersiae (Liliaceae) on acute hepatic failure induced by lipopolysaccharide and D-galactosamine in mice.
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BACKGROUND
This study examined the protective effects of total saponins from Ornithogalum saundersiae (Liliaceae) on D-galactosamine (D-GalN) and lipopolysaccharide (LPS)-induced fulminant hepatic failure.
METHODS
Total saponins of Ornithogalum saundersiae (Liliaceae) (OC) were prepared with ethyl
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
Green tea extract supplement reduces D-galactosamine-induced acute liver injury by inhibition of apoptotic and proinflammatory signaling.
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Oxidative stress and inflammation contributed to the propagation of acute liver injury (ALI). The present study was undertaken to determine whether D-galactosamine (D-GalN) induces ALI via the mitochondrial apoptosis- and proinflammatory cytokine-signaling pathways, and possible mechanism(s) by
Antithrombin III injection via the portal vein suppresses liver damage.
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OBJECTIVE
To investigate the effects of antithrombin III (AT III) injection via the portal vein in acute liver failure.
METHODS
Thirty rats were intraperitoneally challenged with lipopolysaccharide (LPS) and D-galactosamine (GalN) and divided into three groups: a control group; a group injected with
Glycine modulates cytokine secretion, inhibits hepatic damage and improves survival in a model of endotoxemia in mice.
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OBJECTIVE
There is substantial experimental evidence that the amino acid glycine may have a role in protecting tissues against insults such as ischemia, hypoxia and reperfusion. Our aim was to investigate the ability of the amino acid glycine to prevent hepatic damage induced by injection of
[AMPK activator down-regulates the expression of tissue factor in fulminant hepatitis mice].
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AMP activated protein kinase (AMPK) is a pivotal metabolic regulatory enzyme and novel target of controlling inflammation. Our previous studies had demonstrated that 5-amino-4-imidazolecarboxamide riboside (AICAR), an AMPK activator, attenuated lipopolysaccharide (LPS)/D-galactosamine
Ron receptor-dependent gene regulation in a mouse model of endotoxin-induced acute liver failure.
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BACKGROUND
Prior experimentation has shown that loss of the tyrosine kinase (TK) signaling domain of the Ron receptor leads to marked hepatocyte protection in a model of lipopolysaccharide-induced acute liver failure (ALF) in D-galactosamine (GalN)-sensitized mice. The aim of this study was to
Lectin binding sites in normal and phenobarbitale/halothane treated rat liver. A histochemical study.
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The content of carbohydrate residues of both normal and phenobarbitale-halothane-hypoxia exposed rat liver has been examined by means of lectin histochemistry. Eight biotinylated lectins specific to galactose, N-acetyl-galactosamine, N-acetyl-glucosamine, fucose and mannose were applied to paraffin
Mechanisms and mediators in hepatic necrosis.
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Necrotic processes may be restricted to individual cell types of the liver or afflict several liver cells sequentially. Noxious agents may induce necrobiosis by different mechanisms of injury. In many instances, however, similar or identical terminal processes are involved, e.g. accumulation of Ca2+
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