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d galactosamine/cancro
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 320 risultati
Common expression of the tumor marker D-galactose-beta-[1-->3]-N-acetyl-D-galactosamine by different adenocarcinomas: evidence of field effect phenomenon.
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The simple carbohydrate tumor marker D-galactose-beta-[1-->3]-N-acetyl-D-galactosamine (Gal-GalNAc) can be easily identified by a sequential galactose oxidase (GO)-Schiff reaction either on tissues or on rectal mucus samples from patients with colorectal cancer. To check the usefulness of this
Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism.
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OBJECTIVE
The aim was to determine the action mode of cornel iridoid glycoside (CIG) from Fructus corni on hepatoprotective activities, the effects of CIG on human hepatocyte cell line (L02) injured by D-galactosamine (GalN) and tumor necrosis factor-α (TNF-α) were examined.
METHODS
The percentage
Effects of tocotrienol on tumor necrosis factor-α/d-galactosamine-induced steatohepatitis in rats.
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It has been reported that α-tocopherol (α-Toc), a vitamin E analog, is effective for treatment of non-alcoholic steatohepatitis (NASH). However, it is unknown whether or not other vitamin E analogs are effective. Therefore we designed a new rat model of steatohepatitis induced by tumor necrosis
Tumor necrosis factor alpha mediates lethal activity of killed gram-negative and gram-positive bacteria in D-galactosamine-treated mice.
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Treatment with D-galactosamine increases sensitivity of lipopolysaccharide (LPS)-responder mice to the lethal effects of LPS, while nonresponder mice remain resistant (M.A. Freudenberg, D. Keppler, and C. Galanos, Infect. Immun. 51:891-895, 1986). In the present study it is shown that, in contrast
Streptococcus mitis cell walls and lipopolysaccharide induce lethality in D-galactosamine-sensitized mice by a tumor necrosis factor-dependent pathway.
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Purified cells walls of Streptococcus mitis induced tumor necrosis factor in vitro in whole blood of both lipopolysaccharide (LPS)-sensitive OF1 and LPS-resistant C3H/HeJ mice. They were as effective as heat-killed bacteria in inducing death in both strains of mice sensitized with D-galactosamine.
Effects of Z-FA.FMK on D-galactosamine/tumor necrosis factor-alpha-induced kidney injury and oxidative stress in mice : effects of Z-FA.FMK on TNF-alpha-mediated kidney injury.
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BACKGROUND
The aim of this investigation was to demonstrate that benzyloxicarbonyl-L-phenylalanyl-alanine-fluoromethylketone (Z-FA.FMK), which is a pharmacological inhibitor of cathepsin B, has protective role on the kidney injury that occurs together with liver injury. Methods BALB/c male mice used
N-bromoacetyl-beta-D-glucosamine tetra-O-acetate and N-bromoacetyl-beta-D-galactosamine tetra-O-acetate as chemotherapeutic agents with immunopotentiating effects in Ehrlich ascites tumor-bearing mice.
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Protective Effects of Sesquiterpenoids from the Root of Panax ginseng on Fulminant Liver Injury Induced by Lipopolysaccharide/d-Galactosamine.
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It is reported that sesquiterpenoids from Panax ginseng (SPG) possess various pharmacological activities, for example, antidepressant, antioxidative, and anti-inflammatory activities. The purpose of this study was to examine the hepatoprotective effects of SPG (2.5 and 10 mg/kg, i.g.) on fulminant
Esculin prevents Lipopolysaccharide/D-Galactosamine-induced acute liver injury in mice.
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Liver injury is an important cause of serious liver disease and is characterized by inflammatory and oxidative responses. Esculin, a coumarinic derivative found in Aesculus hippocastanum L., has been shown to exhibit anti-inflammatory and anti-oxidative effects. Here, we investigated the effects and
Lectins isolated from Korean mistletoe (Viscum album coloratum) induce apoptosis in tumor cells.
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Cytotoxic lectins (KML-C) were isolated from an extract of Korean mistletoe [Viscum album C. (coloratum)] by affinity chromatography on a hydrolysed Sepharose 4B column, and the chemical and biological properties of KML-C were examined, partly by comparing them with a lectin (EML-1) from European
Pretreatment with Salvia miltiorrhiza Polysaccharides Protects from Lipopolysaccharides/d-Galactosamine-Induced Liver Injury in Mice Through Inhibiting TLR4/MyD88 Signaling Pathway.
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The study was conducted to investigate the protective effects of Salvia miltiorrhiza polysaccharides (SMPs) on lipopolysaccharides (LPS)/d-galactosamine (d-GalN)-induced liver injury in mice and its mechanism. Seventy-two mice were allocated to 6 groups of 12 each, that is, the untreated
Molecular dynamics and binding energy analysis of Vatairea guianensis lectin: a new tool for cancer studies.
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The Tn antigen is an epitope containing N-acetyl-D-galactosamine present in the extracellular matrix of some carcinoma cells in humans, and it is often used as a biomarker. Lectins are proteins capable of binding to carbohydrates and can be used as a molecular tool to recognize antigens and to
Protective effects of morin on lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting TLR4/NF-κB and activating Nrf2/HO-1 signaling pathways.
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Morin, a bioactive flavonoid extracted from the bark of Moraceae plants and many medicinal herbs, has anti-inflammatory and antioxidative effects. In this research, we explored the protective effects of morin against lipopolysaccharide (LPS) and d-galactosamine (D-GalN) induced acute liver injury in
Upregulation of heme oxygenase-1 with hemin prevents D-galactosamine and lipopolysaccharide-induced acute hepatic injury in rats.
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Heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, has been shown to be induced during oxidative injury, and its induction acts as an important cellular defense mechanism against such injuries. In this study, we examined the functional roles of HO-1 induction in a rat model of
Protective Effects of the Third Generation Vasodilatory Βeta - Blocker Nebivolol against D-Galactosamine - Induced Hepatorenal Syndrome in Rats.
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BACKGROUND
Renal dysfunction is very common in patients with advanced liver cirrhosis and portal hypertension. The development of renal failure in the absence of clinical, anatomical or pathological causes renal of failure is termed hepatorenal syndrome (HRS).
OBJECTIVE
The present study was
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