Ginger - An herbal medicinal with broad anti-inflammatory actions

Journal of Medicinal Food Sept 2005

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 anti inflammatory 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.

[6]-Gingerol, a pungent ingredient of ginger, inhibits angiogenesis (cancer) in vitro and in vivo.

Biochem Biophys Res Commun. 2005 Sep Department of Biochemistry, College of Natural Sciences, Yonsei University, Seoul, Republic of Korea.

[6]-Gingerol, a pungent ingredient of ginger (Zingiber officinale Roscoe, Zingiberaceae), has anti-bacterial, anti-inflammatory, and anti-tumor-promoting activities. Here, we describe its novel anti-angiogenic activity in vitro and in vivo. In vitro, [6]-gingerol inhibited both the VEGF- and bFGF-induced proliferation of human endothelial cells and caused cell cycle arrest in the G1 phase. It also blocked capillary-like tube formation by endothelial cells in response to VEGF, and strongly inhibited sprouting of endothelial cells in the rat aorta and formation of new blood vessel in the mouse cornea in response to VEGF. Moreover, i.p. administration, without reaching tumor cytotoxic blood levels, to mice receiving i.v. injection of B16F10 melanoma cells, reduced the number of lung metastasis, with preservation of apparently healthy behavior. Taken together, these results demonstrate that [6]-gingerol inhibits angiogenesis and may be useful in the treatment of tumors and other angiogenesis-dependent diseases.

Morning stiffness and the Anti-Inflammation Diet

Your morning stiffness may not yet qualify as arthritis, but it's likely a sign of inflammation simmering throughout your body. Continue

Ginger extract components suppress induction of chemokine expression in human tissue samples

By the Journal of Alternative Complement Medicine. 2005, Department of Orthopedic Surgery, Division of Arthritis Surgery, Johns Hopkins University, Baltimore, MD.

INTRODUCTION: Ginger has a long history of medicinal use, particularly as an anti-inflammatory agent for a wide variety of diseases such as arthritis. Suppression of inflammation in arthritis is attributed to suppression of pro inflammatory cytokines and chemokines produced by synoviocytes, chondrocytes, and leukocytes. OBJECTIVE: This study aimed to elucidate the effect of a combination ginger extract and its individual components on chemokine expression in human synoviocytes. METHODS: Human synoviocytes were incubated with 100 microg/mL combination ginger extract (GE) of Alpinia galanga (AG) and Zingiber officinale (ZO); AG extract alone; ZO extract alone; or control media, for 1 hour at 37 degrees C, 5% CO2. Cells were next activated with 1 ng/mL of tumor necrosis factor alpha (TNF-alpha) for 1 hour to determine macrophage chemotactic factor (MCP-1) and interferon-gamma activated protein (IP-10) mRNA levels using reverse transcriptase polymerase chain reaction (RT-PCR). Secreted MCP-1 and IP-10 were quantified by enzyme-linked immunosorbent assay (ELISA) following a 24 hour incubation period. RESULTS: The GE combination was consistently more effective in decreasing chemokine mRNA and chemokine secreted protein levels than its individual components ZO or AG. In comparison, ZO was more effective than AG in suppressing chemokine expression. CONCLUSION: The present study demonstrates that GE inhibits chemokine expression, and that the combination of ZO and AG components acts synergistically. This ginger formulation may be useful for suppressing inflammation due to arthritis.

More: Ginger Research

Curcumin, the active constituent of the curry spice, turmeric, inhibits Alzheimer's

"Curcumin (also known as Turmeric) has been used for thousands of years as a safe anti-inflammatory in a variety of ailments as part of Indian traditional medicine," Cole said. Recent animal studies "support a growing interest in its possible use for diseases of aging involving oxidative damage and inflammation like Alzheimer's, cancer and heart disease." Continue

Gamma linolenic acid suppresses inflammation

Gamma Linolenic acid acts as a competitive inhibitor of prostaglandin E2 and leukotrienes (LTs) by reducing the auto-induction of interleukin1alpha (IL-1alpha)-induced pro-IL-1beta gene expression. It appears to be efficacious in rheumatoid arthritis (RA) 15942912&query_hl=22">Semin Arthritis Rheum. 2005 Jun;34(6):773-84.

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