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linoleic acid/necrosis
L'enllaç es desa al porta-retalls
Pàgina 1 des de 300 resultats
Dietary conjugated linoleic acid lowered tumor necrosis factor-alpha content and altered expression of genes related to lipid metabolism and insulin sensitivity in the skeletal muscle of Zucker rats.
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Type-2 diabetes is characterized by obesity-related insulin resistance. Insulin resistance and accompanying hyperinsulinemia have been reported to play an important role in pathogenesis of the metabolic syndrome. Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of
Upregulation of tumor necrosis factor-alpha expression by trans10-cis12 conjugated linoleic acid enhances phagocytosis of RAW macrophages via a peroxisome proliferator-activated receptor gamma-dependent pathway.
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The aim of this study was to examine whether tumor necrosis factor (TNF)-alpha expression in the phagocytic activity of RAW macrophages by trans10-cis12 (10t-12c) conjugated linoleic acid (CLA) is associated with peroxisome proliferator-activated receptor gamma (PPARgamma) activation. 10t-12c CLA
Vitamin E attenuates induction of elastase-like activity by tumor necrosis factor-alpha, cholestan-3 beta,5 alpha,6 beta-triol and linoleic acid in cultured endothelial cells.
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Disturbances in arterial wall elastin metabolism appear to be important factors in atherosclerosis development. To evaluate this hypothesis, elastase-like activity was determined in cultured endothelial cells and their surrounding media after exposure to tumor necrosis factor-alpha (TNF),
Linoleic acid and tumor necrosis factor-alpha increase manganese superoxide dismutase activity in intestinal cells.
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Manganese superoxide dismutase (MnSOD) protects mitochondria from oxidative damage. Alterations in the regulation of MnSOD plays an important role in the development of many types of cancer. Activity of this enzyme is induced by inflammatory cytokines and other conditions that increase oxygen
Dietary conjugated linoleic acid decreased cachexia, macrophage tumor necrosis factor-alpha production, and modifies splenocyte cytokines production.
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The effect of conjugated linoleic acid (CLA) on macrophage functions were studied in vitro, in vivo, and ex vivo. In RAW macrophage cell line, CLA (mixed isomers) was shown to inhibit lipopolysaccharide (LPS)-stimulated tumor necrosis factor-alpha (TNF-alpha) production. Two CLA isomers, c9,t11 and
Trans-10, cis-12-conjugated linoleic acid attenuates tumor necrosis factor-α production by lipopolysaccharide-stimulated porcine peripheral blood mononuclear cells through induction of interleukin-10.
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Conjugated linoleic acid (CLA) can stimulate or inhibit immune cell function, and among CLA isomers, trans-10, cis-12 (t10c12)-CLA was shown to participate in the modulation of pro- or anti-inflammatory cytokine secretion. The objective of this study was to examine the effect of t10c12-CLA on tumor
Effect of conjugated linoleic acid on body fat, tumor necrosis factor alpha and resistin secretion in spontaneously hypertensive rats.
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Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivaties of linoleic acid found mainly in beef and dairy products. CLA has been reported to reduce body fat, as well as to possess anticarcinogenic, antiatherogenic and procatabolic activities in animals. The objective of
Neutrophils from pregnant women produce thromboxane and tumor necrosis factor-alpha in response to linoleic acid and oxidative stress.
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OBJECTIVE
Preeclampsia is associated with oxidative stress, neutrophil activation, neutrophil infiltration into systemic vasculature, and elevated plasma levels of linoleic acid, the fatty acid precursor to arachidonic acid and its metabolite, thromboxane. In this study we evaluated whether linoleic
Zinc protects against apoptosis of endothelial cells induced by linoleic acid and tumor necrosis factor alpha.
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BACKGROUND
Zinc requirements of the vascular endothelium may be increased in inflammatory conditions, ie, atherosclerosis, in which apoptotic cell death is prevalent.
OBJECTIVE
We hypothesized that zinc deficiency may potentiate disruption of endothelial cell integrity mediated by fatty acids and
Conjugated linoleic acid can prevent tumor necrosis factor gene expression by inhibiting nuclear factor binding activity in peripheral blood mononuclear cells from weaned pigs challenged with lipopolysaccharide.
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Twenty-four weanling barrows were fed corn-soybean diets supplemented with 2% conjugated linolenic acid (CLA) or soybean oil. On day 14 and 21, pigs were injected intraperitoneally with lipopolysaccharide (LPS) or sterile saline. Plasma samples were collected 2h after injection. Peripheral blood
Immunoglobulin and cytokine production from spleen lymphocytes is modulated in C57BL/6J mice by dietary cis-9, trans-11 and trans-10, cis-12 conjugated linoleic acid.
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We evaluated the effect of cis-9, trans-11 (9c,11t) and trans-10, cis-12 (10t,12c) conjugated linoleic acid (CLA) on the immune system in C57BL/6J mice. Mice were fed experimental diets containing 0% CLA (controls), 1% 9c,11t-CLA, 1% 10t,12c-CLA or a 1:1 mixture (0.5% + 0.5%) of these two CLA
Conjugated linoleic acid supplementation reduces peripheral blood mononuclear cell interleukin-2 production in healthy middle-aged males.
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Conjugated linoleic acid (CLA) refers to geometric and positional isomers of linoleic acid. Animal studies have shown that CLA modulates the immune system and suggest that it may have a therapeutic role in inflammatory disorders. This double-blind placebo-controlled intervention trial investigated
Linoleic acid prevents chloride influx and cellular lysis in rabbit renal proximal tubules exposed to mitochondrial toxicants.
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Despite many studies elucidating the mechanisms of necrotic cell death, the role of fatty acids released during necrosis remains to be determined. The goals of this study were to determine whether linoleic acid could protect rabbit renal proximal tubules (RPT) from necrotic cell death associated
Application of a continuous bioreactor cascade to study the effect of linoleic acid on hybridoma cell physiology.
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The aim of the present study is to demonstrate the use of controlled bioreactors for toxicological studies. As a model system the effect of linoleic acid on hybridoma cells is studied in two well-controlled continuously operated bioreactors placed in series. In the first reactor the effect on rapid
Histopathologic study of adverse effects of linoleic acid on rat lung.
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Linoleic acid administered intravenously was highly toxic to the rat lung. The severity of the toxicity paralleled the dosage administered and was characterized by generalized, irreversible damage to alveolar wall structures. Although evidence of tissue damage was not apparent or minimal by light
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