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lumicolchicine/betændelse
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12 resultater
Regulation of macrophage collagenase, prostaglandin, and fibroblast-activating-factor production by anti-inflammatory agents: different regulatory mechanisms for tissue injury and repair.
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Activation of macrophages results in the production of tissue destructive mediators and enzymes including prostaglandins (PGE) and collagenase. In addition, activated macrophages also generate mediators which enhance connective tissue formation through their effects on fibroblast growth. To
Colchicine-induced elevation of tissue metallothionein contents is mediated by inflammation-independent serum factor.
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Subcutaneous injection of colchicine caused dose-dependent and time-dependent induction of hepatic MT in mice. Other than colchicine, similar MT induction was observed in vincristine- or vinblastine-injected mice, but not in beta-lumicolchicine-injected mice. MT contents were also elevated in the
Mechanism of action of colchicine : IV. The failure of nonleukopenic doses of colchicine to suppress urate crystal-induced canine joint inflammation.
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Colchicine suppressed the development of urate crystal-induced canine synovitis only at a dose (0.25 mg/kg) that produced a peripheral leukopenia; half that amount produced neither leukopenia nor inhibition of the inflammatory response. Colchicine in the lower dose range still had no
Paradoxical effects of colchicine on the activation of human neutrophilis by chemotactic factors and inflammatory microcrystal.
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Neutrophil activation by chemotactic factors and by inflammatory microcrystals is accompanied by increases in protein tyrosine phosphorylation and by the activation of the NADPH oxidase. The addition of colchicine inhibited both responses induced by triclinic monosodium urate or calcium
Crystal-induced neutrophil activation. III. Inflammatory microcrystals induce a distinct pattern of tyrosine phosphorylation in human neutrophils.
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The activation of human neutrophils by monosodium urate and calcium pyrophosphate dihydrate crystals is believed to play a critical role in the pathogenesis of arthritides such as acute gout and pseudogout, respectively. In this study, we investigated the potential involvement of tyrosine
Microtubule depolymerization selectively down-regulates the synthesis of proinflammatory secretory nonpancreatic phospholipase A2.
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Microtubule depolymerizing agents (MTD) diminish the expression of cell surface receptors for TNF-alpha. Because TNF-alpha along with IL-1 beta markedly enhance the gene expression and extracellular release of proinflammatory secretory nonpancreatic phospholipase A2 (sPLA2), we tested the impact of
Critical review on medicinally potent plant species: Gloriosa superba.
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Gloriosa superba L. is a perennial climber and is used as an ayurvedic medicinal herb to cure diseases in various parts of Africa and Southeast Asia. The plant was under threatened category due to its imprudent harvesting from wild as it is extensively used by medicinal industries for its colchicine
Regulation of guinea pig macrophage collagenase production by dexamethasone and colchicine.
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Previous studies have demonstrated that exposure of guinea pig macrophages to a primary signal, such as lipopolysaccharide (LPS), stimulates the synthesis of prostaglandin E2 (PGE2) which, in turn, elevates cAMP levels resulting in the production of the enzyme, collagenase. The potential of
Colchicine stimulation of pyrogen production by human blood leukocytes.
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The effect of colchicine, an anti-inflammatory agent, on endogenous pyrogen (EP) production by human blood leukocytes in vitro was examined. Colchicine not only failed to suppress EP production by human leukocytes stimulated by phagocytosis, but, in the absence of other stimuli, micromolar
The interaction between lipid derivatives of colchicine and tubulin: consequences of the interaction of the alkaloid with lipid membranes.
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Colchicine is a potent antimitotic poison which is well known to prevent microtubule assembly by binding tubulin very tightly. Colchicine also possesses anti-inflammatory properties which are not well understood yet. Here we show that colchicine tightly interacts with lipid layers. The physical and
Crystal-induced neutrophil activation. IV. Specific inhibition of tyrosine phosphorylation by colchicine.
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We recently demonstrated that pathologically relevant inflammatory microcrystals, namely triclinic monosodium urate (MSU) and calcium pyrophosphate dihydrate (CPPD) crystals, potently stimulate a characteristic protein tyrosine phosphorylation pattern in human neutrophils that differed from that
Colchicine alters the quantitative and qualitative display of selectins on endothelial cells and neutrophils.
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Since colchicine-sensitive microtubules regulate the expression and topography of surface glycoproteins on a variety of cells, we sought evidence that colchicine interferes with neutrophil-endothelial interactions by altering the number and/or distribution of selectins on endothelial cells and
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