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Green tea: a new option for the prevention or control of osteoarthritis

DOI: 10.1186/ar3428

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Abstract:

Inflammation plays a key role in osteoarthritis (OA). The overexpression of cyclooxygenase-2 and proinflammatory cytokines has been reported to contribute to the development of OA. Since chronic inflammation is the leading cause of connective tissue remodeling and destruction in OA, an approach that decreases inflammation may facilitate the development of an effective strategy for its treatment and/or prevention. The use of some drugs has demonstrated potential in treatment of OA but long-term safety, resistance and toxicity concerns have hindered their long-term acceptance as viable clinical chemopreventive agents. The exploration of new agents, particularly dietary, with low toxicity that can target inflammatory responses should form the basis for chemopreventive strategies that will reduce the destruction of cartilage matrix.Green tea polyphenols (GTPs) - a mixture of major polyphenolic constituents found in green tea, including (-)-epicatechin, (-)-epigallocatechin, (-)-epicatechin gallate and (-)-epigallocatechin-3 gallate (EGCG) - offer promising new options for the development of more effective strategies for the prevention of inflammation-associated diseases, including OA. The recent study by Akhtar and Haqqi in Arthritis Research and Therapy indicates that EGCG, the major and most active component of GTPs, protects human chondrocytes from IL-1β-induced inflammatory responses, and suggests the potential of EGCG in OA treatment/prevention [1].Multiple studies were conducted in the research laboratory of Dr Haqqi on the effect of GTPs in arthritis using in vitro and in vivo animal models [2-4]. These studies suggest that GTPs given in drinking water of mice prevented collagen-induced arthritis in the mice, and that this effect of GTPs was associated with the marked reduction of collagen-induced inflammatory mediators such as cyclooxygenase-2 and TNFα in arthritic joints of GTP-fed mice [2]. In vitro studies showed that treatment of human chondrocytes derived f

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