|Shen, Chwan-Li -|
|Yeh, James -|
|Tatum, Owatha -|
|Dagda, Raul -|
|Wang, Jia-Sheng -|
Submitted to: Osteoporosis International
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 14, 2009
Publication Date: November 1, 2010
Repository URL: http://handle.nal.usda.gov/10113/58104
Citation: Shen, C., Yeh, J.K., Cao, J.J., Tatum, O.L., Dagda, R.Y., Wang, J. 2010. Synergistic effects of green tea polyphenols and alphacalcidol on chronic inflammation-induced bone loss in female rats. Osteoporosis International. 21(11):1841-1852. Interpretive Summary: Green tea, one of the most popular beverages in the world, has many beneficial effects on human health, including maintaining bone mass. Green tea extract, GTP (green tea polyphenols), possesses promising antioxidant properties that have been shown to be capable of preventing bone loss in women and men with low bone mass. Vitamin D can be used as a nutritional substitute for mitigating bone loss in osteopenic patients. Vitamin D metabolite, alfacalcidol (1-'-OH-vitamin D3), is more bioavailable than plain vitamin D and has also been shown to mitigate inflammation-induced bone loss. We investigated the potential effects of green tea bioactive components plus alfacalcidol on bone loss in female rats with chronic inflammation. We found that both GTP supplementation and alphacalcidol administration increased bone mineral content and density, decreased serum TRAP levels, urinary 8-hydroxydeoxyguanosine levels, and mRNA expression of tumor necrosis factor-' and cyclooxygenase-2 in spleen. We conclude that GTP or alfacalcidol can prevent bone loss by decreasing oxidative stress and reducing inflammation. Therefore, green tea extract or vitamin D is useful in bone health of patients with chronic inflammation.
Technical Abstract: Summary: Studies suggest that green tea polyphenols (GTP) or alphacalcidol is promising agent for preventing bone loss. Findings that GTP supplementation in the drinking water plus alphacalcidol administration resulted in increased bone mass via a decrease of oxidative stress and inflammation suggest a significant role of GTP plus alphacalcidol in bone health of women with chronic inflammation. Introduction: Recent studies have suggested that green tea polyphenols (GTP) or alphacalcidol are promising dietary supplements for preventing bone loss in women. However, the mechanism(s) related to the possible synergistic osteo-protective role of GTP plus D3 in bone loss due to chronic inflammation is not well understood. Methods: This study evaluated bioavailability, efficacy, and related molecular mechanisms of GTP in combination with alphacalcidol in conserving bone loss in rats with chronic inflammation. A 12-week study of 2 (no GTP vs. 0.5% GTP in drinking water) × 2 (no alphacalcidol vs. 0.05 µg/kg alphacalcidol, 5×/week) factorial design in lipopolysaccharide17 administered female rats was performed. Additionally, a group receiving placebo administration was used to compare with a group receiving lipopolysaccharide administration only to evaluate the effect of lipopolysaccharide. Results: Lipopolysaccharide administration resulted in lower values for bone mineral content and density, but higher values for serum tartrate resistant acid phosphatase (TRAP), urinary 8- hydroxy-2’-deoxyguanosine, and mRNA expression of tumor necrosis factor-a and cyclooxygenase-2 in spleen. GTP supplementation increased urinary epigallocatechin and epicatechin concentrations. Both GTP supplementation and alphacalcidol administration resulted in a significant increase in bone mineral content and density, but a significant decrease in serum TRAP levels, urinary 8-hydroxydeoxyguanosine levels, and mRNA expression of tumor necrosis factor-a and cyclooxygenase-2 in spleen. A synergistic effect of GTP and alphacalcidol was observed in these parameters. Neither GTP nor alphacalcidol affected femoral bone area or serum osteocalcin. Conclusion: We conclude that a bone-protective role of GTP plus alphacalcidol during chronic10 inflammation bone loss may be due to a reduction of oxidative stress damage and inflammation.