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        Ginger-An Herbal Medicinal Product with Broad Anti-Inflammatory Actions

        Carmelita G. Frondoza,Lars Lindmark,Reinhard Grzanna 한국식품영양과학회 2005 Journal of medicinal food Vol.8 No.2

        The anti-inflammatory properties of ginger have been known and valued for centuries. During the past 25years, many laboratories have provided scientific support for the long-held belief that ginger contains constituents with anti-inflammatory properties. The original discovery of ginger’s inhibitory effects on prostaglandin biosynthesis in the early 1970shas been repeatedly confirmed. This discovery identified ginger as an herbal medicinal product that shares pharmacologicalproperties with non-steroidal anti-inflammatory drugs. Ginger suppresses prostaglandin synthesis through inhibition of cy-clooxygenase-1 and cyclooxygenase-2. An important extension of this early work was the observation that ginger also sup-presses leukotriene biosynthesis by inhibiting 5-lipoxygenase. This pharmacological property distinguishes ginger from non-steroidal anti-inflammatory drugs. This discovery preceded the observation that dual inhibitors of cyclooxygenase and5-lipoxygenase may have a better therapeutic profile and have fewer side effects than non-steroidal anti-inflammatory drugs.The characterization of the pharmacological properties of ginger entered a new phase with the discovery that a ginger extract(EV.EXT.77) derived from Zingiber officinale(family Zingiberaceae) and Alpina galanga (family Zingiberaceae) inhibits theinduction of several genes involved in the inflammatory response. These include genes encoding cytokines, chemokines, andthe inducible enzyme cyclooxygenase-2. This discovery provided the first evidence that ginger modulates biochemical path-ways activated in chronic inflammation. Identification of the molecular targets of individual ginger constituents provides anopportunity to optimize and standardize ginger products with respect to their effects on specific biomarkers of inflammation.Such preparations will be useful for studies in experimental animals and humans.

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        Avocado/Soybean Unsaponifiables, Glucosamine and Chondroitin Sulfate Combination Inhibits Proinflammatory COX-2 Expression and Prostaglandin E2 Production in Tendon-Derived Cells

        Mark W. Grzanna,Rebecca Y. Au,Angela Y. Au,Ann M. Rashmir,Carmelita G. Frondoza 한국식품영양과학회 2020 Journal of medicinal food Vol.23 No.2

        Tendinopathy, a common disorder in man and horses, is characterized by pain, dysfunction, and tendon degeneration. Inflammation plays a key role in the pathogenesis of tendinopathy. Tendon cells produce proinflammatory molecules that induce pain and tissue deterioration. Currently used nonsteroidal anti-inflammatory drugs are palliative but have been associated with adverse side effects prompting the search for safe, alternative compounds. This study determined whether tendon-derived cells' expression of proinflammatory cyclooxygenase (COX)-2 and production of prostaglandin E2 (PGE2) could be attenuated by the combination of avocado/soybean unsaponifiables (ASU), glucosamine (GLU), and chondroitin sulfate (CS). ASU, GLU, and CS have been used in the management of osteoarthritis-associated joint inflammation. Tenocytes in monolayer and microcarrier spinner cultures were incubated with media alone, or with the combination of ASU (8.3 μg/mL), GLU (11 μg/mL), and CS (20 μg/mL). Cultures were next incubated with media alone, or stimulated with interleukin-1β (IL-1β; 10 ng/mL) for 1 h to measure COX-2 gene expression, or for 24 h to measure PGE2 production, respectively. Tenocyte phenotype was analyzed by phase-contrast microscopy, immunocytochemistry, and Western blotting. Tendon-derived cells proliferated and produced extracellular matrix component type I collagen in monolayer and microcarrier spinner cultures. IL-1β-induced COX-2 gene expression and PGE2 production were significantly reduced by the combination of (ASU+GLU+CS). The suppression of IL-1β-induced inflammatory response suggests that (ASU+GLU+CS) may help attenuate deleterious inflammation in tendons.

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