Dietary administration of Curcumin modifies transcriptional profile of genes involved in inflammatory cascade in horse leukocytes
Pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor- alpha (TNF-α) play a key role in the pathogenesis of osteoarthritis (OA). Once released, these cytokines are potent stimulators for the de novo production of catabolic enzymes such as matrix metalloproteinases (MMPs...
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Veröffentlicht in: | Italian journal of animal science 2009-01, Vol.8 (sup2), p.84-86 |
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Sprache: | eng |
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Zusammenfassung: | Pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor- alpha (TNF-α) play a key role in the pathogenesis of osteoarthritis (OA). Once released, these cytokines are potent stimulators for the de novo production of catabolic enzymes such as matrix metalloproteinases (MMPs) and cyclo-oxygenase-2 (COX-2). Anti-inflammatory agents capable of suppressing the production and catabolic actions of these cytokines may have therapeutic potential in the treatment of OA and a range of other osteoarticular disorders. The purpose of this study was to examine the therapeutic effect of Curcumin (diferuloylmethane), a pharmacologically safe phytochemical agent, on males and foals affected by degenerative joint diseases. Curcumin, in the form phytosome (CURCUVET
®
, Indena Spa, Milan, Italy) was administered to animals for fifteen days and gene expression was monitored before the treatment and after four, eight, and fifteen days. In mares, Curcumin inhibited the expression of COX-2, TNF-α, IL-1β, IL1RN, and IL6, even if only the downregulation of IL-1β and IL1RN were significant. In foals, Curcumin significantly inhibited the expression of COX-2, TNF-α, IL1RN and significantly increased that of IL6. These results indicate that Curcumin has nutritional potential as a natural anti-inflammatory agent for treating osteoarticular disorders through suppression of pro-inflammatory cytokines and catabolic enzymes. |
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ISSN: | 1828-051X 1594-4077 1828-051X |
DOI: | 10.4081/ijas.2009.s2.84 |