galactosamine/inflammation

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An ultrastructural and histochemical study of the prominent inflammatory response in D(+)-galactosamine hepatotoxicity.

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The biochemical basis of the hepatitis-like liver injury produced by D(+)-galactosamine in rats is well-established and is linked to depletion of uridine nucleotides within parenchymal cells. However, the prominent inflammatory response that accompanies this lesion in vivo has been largely

Antileukoproteinase protects against hepatic inflammation, but not apoptosis in the response of D-galactosamine-sensitized mice to lipopolysaccharide.

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OBJECTIVE There is major evidence for the strong bi-directional interrelation of parenchymal cell apoptosis and leukocyte accumulation and inflammation in acute liver injury. Therefore, the aim of this in vivo study was to investigate the anti-apoptotic and anti-inflammatory potential of

Propofol attenuates inflammatory response and apoptosis to protect d-galactosamine/lipopolysaccharide induced acute liver injury via regulating TLR4/NF-κB/NLRP3 pathway.

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Propofol has been reported to be protective against liver injury due to its anti-inflammatory, anti-oxidative and anti-apoptotic activities. The purpose of this study was to examine the protective effects of propofol on d-galactosamine/lipopolysaccharide (d-GalN/LPS) induced acute

Crocetin protects against fulminant hepatic failure induced by lipopolysaccharide/D-galactosamine by decreasing apoptosis, inflammation and oxidative stress in a rat model.

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Fulminant hepatic failure (FHF) is a clinical syndrome characterized by sudden and severe liver dysfunction. Apoptosis and inflammation are essential for the pathogenesis of FHF. Crocetin, the major component present in saffron, has been reported to possess anti-inflammatory and antioxidant

A mixture of mulberry and silk amino acids protected against D-galactosamine induced acute liver damage by attenuating oxidative stress and inflammation in HepG2 cells and rats.

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The liver is an important organ for the removal of toxins and utilization of nutrients. The present study then investigated whether a mixture of mulberry water extracts and silk amino acids protected against acute liver damage in rats induced by intraperitoneal injection of D-galactosamine and the

In vitro inhibition of lipopolysaccharide and mycobacterium bovis bacillus Calmette Guérin-induced inflammatory cytokines and in vivo protection from D-galactosamine/LPS -mediated liver injury by the medicinal plant Sclerocarya birrea.

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Sclerocarya birrea is a medicinal plant used for the treatment of inflammatory- and bacterial-related diseases. The present study investigated in vitro and in vivo the effects of the stem bark methanol extract of S. birrea. Nitrite, TNF, IL-1beta, IL-6 and IL-12p40 production by bone marrow-derived

[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

The anti-inflammatory effects of ethyl acetate on Lipopolysaccharide/D-galactosamine challenged mice and Lipopolysaccharide activated RAW264.7 cells.

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Ethyl acetate (EA) is an ordinary organic compound in fruits, wine and cosmetics, and used as a solvent frequently. With the recent observation in our experiment, we suspected that EA could affect immune function, in particular macrophage activity. In this paper, we tested EA's protect effect

Suppression of lipopolysaccharide and galactosamine-induced hepatic inflammation by red grape pomace.

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Grape pomace is generated in the production process of wine and grape juices and is an industrial waste. This study investigated whether an intake of grape pomace was able to suppress chronic inflammation induced by lipopolysaccharide (LPS) and galactosamine (GalN) in vivo. When Sprague-Dawley rats

Methylprednisolone injection via the portal vein suppresses inflammation in acute liver failure induced in rats by lipopolysaccharide and d-galactosamine.

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BACKGROUND We have reported that hepatic arterial steroid injection is an effective therapy to rescue patients from fulminant or severe acute hepatic failure. We speculate that a high concentration of steroid suppresses inflammatory processes in the liver directly by restraining activated

Chicoric acid ameliorate inflammation and oxidative stress in Lipopolysaccharide and d-galactosamine induced acute liver injury.

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Chicoric acid is polyphenol of natural plant and has a variety of bioactivity. Caused by various kinds of stimulating factors, acute liver injury has high fatality rate. The effect of chicoric acid in acute liver injury induced by Lipopolysaccharide (LPS) and d-galactosamine (d-GalN) was

β-Hydroxybutyrate exacerbates lipopolysaccharide/ d-galactosamine-induced inflammatory response and hepatocyte apoptosis in mice.

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β-Hydroxybutyrate (BHB), one of ketone body, has been traditionally regarded as an alternative carrier of energy, but recent studies found that BHB plays versatile roles in inflammation. It has been previously reported that the level BHB declined in mice with lipopolysaccharide (LPS)/d-galactosamine

Tamoxifen Attenuates Lipopolysaccharide/Galactosamine-induced Acute Liver Failure by Antagonizing Hepatic Inflammation and Apoptosis.

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Bacterial lipopolysaccharide (LPS)-induced acute liver failure (ALF) is a common severe clinical syndrome in intensive care unit. No other methods are available for its prevention apart from supportive treatment and liver transplantation. Tamoxifen (TAM) was reported to attenuate ALF induced by

Protective effects of alpinetin on lipopolysaccharide/d-Galactosamine-induced liver injury through inhibiting inflammatory and oxidative responses.

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Alpinetin, a type of novel plant flavonoid derived from Alpinia katsumadai Hayata, has been reported to have anti-inflammatory effects. The aim of this investigation was designed to reveal the protective effects of alpinetin on Lipopolysaccharide (LPS)/d-galactosamine (D-Gal)-induced liver injury in

Protective effects of oxymatrine against lipopolysaccharide/D‑galactosamine‑induced acute liver failure through oxidative damage, via activation of Nrf2/HO‑1 and modulation of inflammatory TLR4‑signaling pathways.

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Oxymatrine has a variety of pharmacological functions, including anti-viral, anti-liver fibrotic, anti-cancer, anti‑bacterial, anti‑epidemic, analgesic, anti‑allergy and anti‑inflammatory properties. The present study aimed to investigate the protective effects of oxymatrine against

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