|SHEN, CHWAN-LI - TEXAS TECH UNIVERSITY|
|YEH, JAMES - WINTHROP UNIVERSITY HOSPITAL|
|TATUM, OWATHA - TEXAS TECH UNIVERSITY|
|DAGDA, RAUL - TEXAS TECH UNIVERSITY|
|WANG, JIA-SHENG - UNIVERSITY OF GEORGIA|
Submitted to: Journal of Nutritional Biochemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/12/2009
Publication Date: 10/1/2010
Citation: Shen, C., Yeh, J.K., Cao, J.J., Tatum, O.L., Dagda, R.Y., Wang, J. 2010. Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model. Journal of Nutritional Biochemistry. 21(10):968-974.
Interpretive Summary: Bone loss is associated with oxidative stress in animal and humans. Oxidative stress results from high levels of reactive oxygen species (ROS). ROS can cause severe damage to DNA, protein, and lipids. Oxidative stress may also contribute to bone loss due to chronic inflammation. Green tea as the most popular beverage in the world has many health benefits to humans including supporting bone health. The present study was designed to investigate the effects of green tea or green tea bioactive components on chronic-inflammation-induced bone loss and related molecular mechanism(s). We found that lipopolysaccharide administration decreased femur BMC and BMD, and serum osteocalcin levels, but increased serum TRAP, urinary 8-OHdG, and spleen mRNA expression of TNF-a and COX-2 levels. Green tea polyphenol supplementation increased urinary epigallocatechin and epicatechin concentrations, increased femur BMC, BMD and serum osteocalcin, but decreased serum TRAP, urinary 8-OHdG, and spleen mRNA expression of TNF-a and COX-2 levels. Our data suggest that green tea polyphenol supplementation mitigates bone loss in a chronic-inflammation-induced bone loss model by reducing oxidative stress-induced damage and inflammation.
Technical Abstract: The purpose of this study was to explore 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) × 2 (no GTP vs. 0.5% GTP in drinking water) factorial design using 40 female rats (3-month-old) assigned to 4 groups for 12 weeks. 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-a (TNF-a) and cyclooxygenase-2 (COX-2) in spleen was determined by real-time RT-PCR. Neither LPS administration nor GTP levels affected body weight 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-a 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-a and COX-2levels. We conclude that GTP mitigates bone loss in a chronic-inflammation-induced bone loss 20 model by reducing oxidative stress-induced damage and inflammation.