4.7 Article

Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model

期刊

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 21, 期 10, 页码 968-974

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2009.08.002

关键词

Tea; Dietary supplement; Inflammation; Bone; Oxidative stress

资金

  1. Laura W. Bush Institute for Women's Health
  2. NIH/NCCAM [R21AT003735]
  3. NIH/NCI [CA90997]

向作者/读者索取更多资源

The purpose of this study was to explore the bioavailability, efficacy and molecular mechanisms of green tea polyphenols (GTP) related to preventing bone loss in rats with chronic inflammation. A 2 [placebo vs. lipopolysaccharide (LPS)]x2 (no GTP vs. 0.5% GTP in drinking water) factorial design enabled the evaluation of effects of LPS administration, GTP levels, and LPSxGTP interaction. Urinary GTP components and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were determined by high-pressure liquid chromatography for bioavailability and molecular mechanism, respectively. Efficacy was evaluated by examining changes in femoral mineral content (BMC) and density (BMD) using dual-energy X-ray absorptiometry, and bone turnover biomarkers [osteocalcin (OC) and tartrate-resistant acid phosphatase (TRAP)] using respective ELISA kits. The mRNA expression of tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase-2 (COX-2) in spleen was determined by real-time RT-PCR. Neither LPS administration nor GTP levels affected body weight and femoral bone area throughout the study period. Only GTP supplementation resulted in increased urinary epigallocatechin and epicatechin concentrations. LPS administration led to a decrease in femur BMC and BMD, and serum OC levels, but an increase in serum TRAP, urinary 8-OHdG and spleen mRNA expression of TNF-alpha and COX-2 levels. GTP supplementation resulted in higher values for femur BMC, BMD and serum OC, but lower values for serum TRAP, urinary 8-OHdG and spleen mRNA expression of TNF-alpha and COX-2 levels. We conclude that GTP mitigates bone loss in a chronic inflammation-induced bone loss model by reducing oxidative stress-induced damage and inflammation. (C) 2010 Elsevier Inc. All rights reserved.

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