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

      1 , 2 , 3
      Journal of Medicinal Food
      Mary Ann Liebert Inc

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          Abstract

          The anti-inflammatory properties of ginger have been known and valued for centuries. During the past 25 years, many laboratories have provided scientific support for the long-held belief that ginger contains constituents with antiinflammatory properties. The original discovery of ginger's inhibitory effects on prostaglandin biosynthesis in the early 1970s has been repeatedly confirmed. This discovery identified ginger as an herbal medicinal product that shares pharmacological properties with non-steroidal anti-inflammatory drugs. Ginger suppresses prostaglandin synthesis through inhibition of cyclooxygenase-1 and cyclooxygenase-2. An important extension of this early work was the observation that ginger also suppresses leukotriene biosynthesis by inhibiting 5-lipoxygenase. This pharmacological property distinguishes ginger from nonsteroidal anti-inflammatory drugs. This discovery preceded the observation that dual inhibitors of cyclooxygenase and 5-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 the induction of several genes involved in the inflammatory response. These include genes encoding cytokines, chemokines, and the inducible enzyme cyclooxygenase-2. This discovery provided the first evidence that ginger modulates biochemical pathways activated in chronic inflammation. Identification of the molecular targets of individual ginger constituents provides an opportunity 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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          Most cited references57

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          Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.

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            Cytokine pathways and joint inflammation in rheumatoid arthritis.

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              Cyclooxygenases 1 and 2.

              Cyclooxygenase (COX), first purified in 1976 and cloned in 1988, is the key enzyme in the synthesis of prostaglandins (PGs) from arachidonic acid. In 1991, several laboratories identified a product from a second gene with COX activity and called it COX-2. However, COX-2 was inducible, and the inducing stimuli included pro-inflammatory cytokines and growth factors, implying a role for COX-2 in both inflammation and control of cell growth. The two isoforms of COX are almost identical in structure but have important differences in substrate and inhibitor selectivity and in their intracellular locations. Protective PGs, which preserve the integrity of the stomach lining and maintain normal renal function in a compromised kidney, are synthesized by COX-1. In addition to the induction of COX-2 in inflammatory lesions, it is present constitutively in the brain and spinal cord, where it may be involved in nerve transmission, particularly that for pain and fever. PGs made by COX-2 are also important in ovulation and in the birth process. The discovery of COX-2 has made possible the design of drugs that reduce inflammation without removing the protective PGs in the stomach and kidney made by COX-1. These highly selective COX-2 inhibitors may not only be anti-inflammatory but may also be active in colon cancer and Alzheimer's disease.
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                Author and article information

                Journal
                Journal of Medicinal Food
                Journal of Medicinal Food
                Mary Ann Liebert Inc
                1096-620X
                1557-7600
                June 2005
                June 2005
                : 8
                : 2
                : 125-132
                Affiliations
                [1 ]RMG Biosciences, Inc.
                [2 ]Ferrosan A/S, Soeborg, Denmark.
                [3 ]Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
                Article
                10.1089/jmf.2005.8.125
                16117603
                347ee00a-9ffc-40bc-9b1f-4df8138710da
                © 2005

                http://www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/

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