d galactosamine/edema

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The appearance of D-galactosamine-induced hepatitis and generalized edema in adrenalectomized rats.

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In adrenalectomized female rats a single dose of 375 mg D-galactosamine.HCl per kg of body weight produces both hepatitis and generalized edema with ascites. These alterations depend upon the dose and the time interval after injection of the aminosugar. The effect is specific for D-galactosamine;

Hemodynamic, biochemical and morphological changes in the dextran and D-galactosamine-induced edemas in rats.

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Dextran (600 mg/kg i.p.) and D-galactosamine (300 mg/kg s.c.)-induced edemas in the rat have been evaluated and compared on the basis of hemodynamic, biochemical and morphological investigations. The genesis of the edema induced by dextran was quicker (1-3 hr) than that induced by D-galactosamine.

Induction of edema in the adrenalectomized rat by D-galactosamine.

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Effects of D-galactosamine-induced acute liver injury on mortality and pulmonary responses to Escherichia coli lipopolysaccharide. Modulation by arachidonic acid metabolites.

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Multiple extrapulmonary organ system failures increase mortality, permeability edema, and alveolar inflammation during gram-negative sepsis because of abnormal regulation of host inflammatory responses. We tested the hypothesis that acute hepatocytic injury induced by the selective hepatotoxin,

[Protective effect of the histone deacetylase inhibitor ACY1215 against brain edema in mice with acute liver failure].

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Objective: To investigate the protective effect of ACY1215 (Rocilinostat), a histone deacetylase inhibitor, against brain edema in mice with acute liver failure. Methods: Lipopolysaccharide combined with D-galactosamine was used to establish a mouse model of acute liver failure, and ACY1215 was used

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)

TIMP-1/MMP-9 imbalance in brain edema in rats with fulminant hepatic failure.

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BACKGROUND Fulminant hepatic failure (FHF) is a devastating disease. When coma sets in, brain edema develops, changing FHF into a lethal condition. Liver transplantation is the definitive treatment. However, a third of these patients die as the result of brain edema before a donor becomes available.

Brain expression of the water channels aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema.

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Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or

Palmatine attenuates D-galactosamine/lipopolysaccharide-induced fulminant hepatic failure in mice.

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Palmatine is an isoquinoline alkaloid from Coptis chinensis, an herbal medicine used to treat various inflammatory diseases such as gastritis, edema and dermatitis. The present study examined the cytoprotective properties of palmatine on d(+)-galactosamine (GalN)/lipopolysaccharide (LPS)-induced

Cerebral edema in the rat with galactosamine induced severe hepatitis.

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With D-galactosamine hydrochloride severe hepatitis was induced in rats and the water content of cerebrum, cerebellum and brain stem determined. The animals showed a parallel increase in cerebral water content and occurrence of cerebral symptoms.

Effectivity and safety of mannitol treatment for acute hepatic failure in rats.

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In rats with D-galactosamine-induced hepatic failure, 14C-D-mannitol transport into the brain was accelerated through an increase of vesicular transport via the blood-brain barrier and thus brain mannitol contents increased. However, the osmolarity of the brain tissue changed little and the

Neurokinin-1 receptor antagonists CP-96,345 and L-733,060 protect mice from cytokine-mediated liver injury.

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Previously, we have shown that primary afferent sensory neurons are necessary for disease activity in T cell-mediated immune hepatitis in mice. In the present study, we analyzed the possible role of substance P (SP), an important proinflammatory neuropeptide of these nerve fibers, in an in vivo

The anti-inflammatory and hepatoprotective effects of fractions from Cudrania cochinchinensis var. gerontogea.

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Various fractions of the ethanol extract from the root wood of Cudrania cochinchinensis var. gerontogea (Moraceae) were evaluated for their anti-inflammatory effects on carrageenan-induced edema and hepatoprotective activities on carbon tetrachloride (CCl4)-induced and D-galactosamine-(D-GalN)

The antiinflammatory and liver protective effects of Boehmeria nivea and B. nivea subsp. nippononivea in rats.

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The pharmacological effects of Boehmeria nivea and B. nivea subsp. nippononivea were studied against carrageenan-induced paw edema, acetaminophen (APAP) and D-galactosamine (D-GalN) induced hepatotoxicity in rats, respectively. Water extracts of B. nivea and B. nivea subsp. nippononivea roots were

Contribution of the carbohydrate-binding ability of Vatairea guianensis lectin to induce edematogenic activity.

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Vatairea guianensis lectin (VGL), Dalbergiae tribe, is a N-acetyl-galactosamine (GalNAc)/Galactose (Gal) lectin previously purified and characterized. In this work, we report its structural features, obtained from bioinformatics tools, and its inflammatory effect, obtained from a rat paw edema

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