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d fructose/nécrose
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The effect of tumor necrosis factor-alpha on D-fructose intestinal transport in rabbits.
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Tumor necrosis factor-alpha (TNF-alpha) is an important immunoregulatory cytokine involved in septic responses during bacterial infection. The aim of this study was to examine the effect of TNF-alpha on the transport of D-fructose across rabbit jejunum. A sepsis condition was evoked by intravenous
Dimethyl sulfoxide activates tumor necrosis factorα-p53 mediated apoptosis and down regulates D-fructose-6-phosphate-2-kinase and lactate dehydrogenase-5 in Dalton's lymphoma in vivo.
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Dimethyl sulfoxide (DMSO) is evident to induce apoptosis in certain tumor cells in vitro. However, its apoptotic mechanism remains unexplored in in vivo tumors. This article describes that DMSO, being non-toxic to the normal lymphocytes, up regulated TNFα and p53, declined Bcl-2/Bax ratio, activated
Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum.
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OBJECTIVE
To investigate alterations in the transport of D-fructose across the rabbit jejunum when the gut is exposed in vitro to lipopolysaccharide (LPS), an endotoxin causative agent of sepsis.
METHODS
D-fructose intestinal transport was assesed employing three techniques: sugar uptake
1,5-Anhydro-D-fructose attenuates lipopolysaccharide-induced cytokine release via suppression of NF-kappaB p65 phosphorylation.
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Lipopolysaccharide (LPS) stimulates macrophages by activating NF-kappaB, which contributes to the release of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6. 1,5-Anhydro-D-fructose (1,5-AF), a monosaccharide formed from starch and glycogen, exhibits anti-oxidant activity and enhances
Di-D-fructose dianhydride-enriched caramels: effect on colon microbiota, inflammation, and tissue damage in trinitrobenzenesulfonic acid-induced colitic rats.
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In the present study we describe the preparation and chemical characterization of a caramel with a high (70%) content of difructose dianhydrides (DFAs) and glycosylated derivatives (DFAs). This product was obtained by thermal activation (90 degrees C) of highly concentrated (90% w/v) aqueous
Inhibitory effect of TNF-alpha on the intestinal absorption of galactose.
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Sepsis is a systemic response to infection in which toxins, such as bacterial lipopolysaccharide (LPS), stimulate the production of inflammatory mediators like the cytokine tumor necrosis factor alpha (TNF-alpha). Previous studies from our laboratory have revealed that LPS inhibits the intestinal
Fructose-1,6-bisphosphate reduces inflammatory pain-like behaviour in mice: role of adenosine acting on A1 receptors.
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OBJECTIVE
D-Fructose-1,6-bisphosphate (FBP) is an intermediate in the glycolytic pathway, exerting pharmacological actions on inflammation by inhibiting cytokine production or interfering with adenosine production. Here, the possible antinociceptive effect of FBP and its mechanism of action in the
Studies on severe hepatic damage induced by galactosamine.
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Severe hepatic damage with submassive necrosis induced in rats by an intraperitoneal injection of a single dose of galactosamine hydrochloride was studied. In the severely damaged liver, the remarkable decreases of glycogen and UDPG in the damaged liver were seen. This means extreme decrease in the
Studies on streptozotocin diabetes.
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Both alloxan and streptozotocin produce beta-cell necrosis in the rat. Previous studies have shown protection against alloxan toxicity by D-glucose, D-mannose, and the nonmetabolized analogue 3-0-methyl-D-glucose and removal of this protective effect by D-mannoheptulose. The effect of several agents
Exercise training modulates the hepatic renin-angiotensin system in fructose-fed rats.
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What is the central question of this study? What are the effects of exercise training on the hepatic renin-angiotensin system and their contribution to damage resulting from fructose overload in rats? What is the main finding and its importance? Exercise training attenuated the deleterious actions
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