d 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

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

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

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+

HIF1a Inhibitor Rescues Acute-on-Chronic Liver Failure.

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Hypoxia-inducible factor-1α is critically involved in the pathogenesis of liver diseases. Its inhibitor genistein attenuated D-galactosamine (D-GalN)-induced liver damage. However, the role of genistein in acute-on-chronic liver failure (ACLF) is unclear. The influence of genistein on

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