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carrageenan/некроза
Веза се чува у привремену меморију
Страна 1 од 531 резултати
Contribution of neutrophils to lipopolysaccharide-induced tumor necrosis factor production and mortality in a carrageenan-pretreated mouse model.
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Carrageenan (CAR) pretreatment primes mice for lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-alpha production in sera and increases their mortality rate. To study the contribution of neutrophils in this model, blood neutrophil count was regulated with cyclophosphamide. After LPS
Effects of a bupivacaine nerve block on the axonal transport of Tumor Necrosis Factor-alpha (TNF-alpha) in a rat model of carrageenan-induced inflammation.
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Many pro-inflammatory cytokines are involved in the process of inflammatory pain. Bi directional axonal transport of Tumor Necrosis Factor-alpha (TNF-alpha) occurs in case of neuropathic pain induced by nerve ligation. We used an in vivo preparation with injection of carrageenan and fluorescent
Enhancement of lipopolysaccharide-induced tumor necrosis factor production in mice by carrageenan pretreatment.
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Tumor necrosis factor (TNF) is a cytokine which mediates endotoxin shock and causes multiple organ damage. It is thought that macrophage (MP) activation is necessary to increase lipopolysaccharide (LPS)-induced TNF production and lethality. Carrageenan (CAR) is sulfated polygalactose which destroys
An antagonist of platelet-activating factor suppresses endotoxin-induced tumor necrosis factor and mortality in mice pretreated with carrageenan.
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We found that carrageenan (CAR), that is, sulfated polygalactose, can enhance both lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF) production and the rate of lethality in mice (M. Ogata, S. Yoshida, M. Kamochi, A. Shigematsu, and Y. Mizuguchi, Infect. Immun. 59:679-683, 1991). It has
Carrageenan-induced acute inflammation in the mouse air pouch synovial model. Role of tumour necrosis factor.
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We used the mouse air pouch model of inflammation to study the interaction between cytokines, prostaglandin E(2) (PGE(2)) and cell migration during the various phases of acute local inflammation induced by carrageenan. In serum, the levels of interleukin 1 (IL-1), interleukin 6 (IL-6), tumour
A model of peripheral microvascular injury: irreversible caudal necrosis induced in carrageenan-inflamed rats treated with anti-inflammatory drugs and mild chilling: a pluricausal thrombo-haemorrhagic phenomenon.
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A florid tail injury was observed in carrageenan-inflamed rats previously treated with acidic non-steroidal anti-inflammatory (NSAI) drugs to suppress paw inflammation and then exposed to mild chilling (7-10 degrees C for 10-16 h). All three treatments, i.e. NSAI drug + carrageenan paw oedema + mild
Carrageenan primes leukocytes to enhance lipopolysaccharide-induced tumor necrosis factor alpha production.
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We have previously reported that pretreatment with carrageenan (CAR) enhances lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) production in and lethality for mice. Whole blood cultured in vitro was used to show that CAR pretreatment results in about a 200-fold increase in
Effect of tumour necrosis factor-alpha receptor 1 genetic deletion on carrageenan-induced acute inflammation: a comparison with etanercept.
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In the present study, we used tumour necrosis factor-alpha receptor 1 knock-out mice (TNF-alphaR1KO) to evaluate an in vivo role of TNF-alphaR1 on the pathogenesis of inflammatory diseases. We used a murine model of carrageenan-induced acute inflammation (pleurisy), a preclinical model of airway
Relevance of tumour necrosis factor-alpha for the inflammatory and nociceptive responses evoked by carrageenan in the mouse paw.
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1. The present study evaluated the participation of tumour necrosis factor-alpha (TNF-alpha) in the inflammatory and nociceptive responses evoked by carrageenan in the mouse paw. 2. The intraplantar injection of carrageenan (300 microg paw-1) induced a marked and biphasic paw oedema formation (peaks
Tumor necrosis factor alpha-induced inflammation is increased but apoptosis is inhibited by common food additive carrageenan.
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Tumor necrosis factor (TNF)-α, a homotrimeric, pleiotropic cytokine, is secreted in response to inflammatory stimuli in diseases such as rheumatoid arthritis and inflammatory bowel disease. TNF-α mediates both apoptosis and inflammation, stimulating an inflammatory cascade through the non-canonical
Ketamine suppresses tumor necrosis factor-alpha activity and mortality in carrageenan-sensitized endotoxin shock model.
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We have reported that an intravenous anesthetic, ketamine, has a potent suppressive effect on lipopolysaccharide (LPS)-induced TNF-alpha production in vitro [Takenaka et al., Anesthesiology 80:402-408, 1994]. The purpose of the present study was to investigate the overall effects of ketamine on
Sclareol exhibits anti-inflammatory activity in both lipopolysaccharide-stimulated macrophages and the λ-carrageenan-induced paw edema model.
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Sclareol (1) is a natural fragrance compound used widely in the cosmetic and food industries. Lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and the λ-carrageenan-induced edema mouse paw model were applied to examine the anti-inflammatory potential of 1 and its possible molecular
Oral treatment of rats with bovine lactoferrin inhibits carrageenan-induced inflammation; correlation with decreased cytokine production.
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The aim of this study was to investigate an effect of oral treatment of rats with bovine lactoferrin (BLF) on carrageenan-induced inflammation. Rats were given 5 oral doses of BLF (10 mg each) on alternate days and 24 h after the last dose a carrageenan inflammation was induced in the hind foot.
Evidence of anti-inflammatory effects of pioglitazone in the murine pleurisy model induced by carrageenan.
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Several studies have shown that the anti-inflammatory effect of Pioglitazone extends beyond the cardiovascular system. This study examines the anti-inflammatory effect of Pioglitazone in comparison to reference drugs (Dexamethasone and Indomethacin) in the mouse model of pleurisy induced by
Gold nanoparticles and/or N-acetylcysteine mediate carrageenan-induced inflammation and oxidative stress in a concentration-dependent manner.
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We report the effect of gold nanoparticles (AuNP) in an acute inflammation model induced by carrageenan (CG) and compared this effect with those induced by the antioxidant N-acetylcysteine (NAC) alone and by the synergistic effect of NAC and AuNP together. Male Wistar rats received saline or saline
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