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Title:   Author  item
                                            SHEN, CHWAN-LI - Texas Tech Universityitem
                                            YEH, JAMES - Winthrop University Hospitalitem
                                            SAMATHANAM, CHRISTINA - Texas Tech Universityitem
                                            Cao, Jayitem
                                            STOECKER, BARBARA - Oklahoma State Universityitem
                                            DAGDA, RAU - Texas Tech Universityitem
                                            CHYU, MING-CHIEN - Texas Tech Universityitem
                                            WANG, JIA-SHENG - University Of Georgia
  Submitted to: Journal of Nutritional Biochemistry
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 5/29/2010
                                    Publication  Date: 6/1/2011
                                    Citation: Shen, C., Yeh, J.K., Samathanam, C.A., Cao, J.J., Stoecker, B.J., Dagda, R.Y., Chyu, M., Wang, J. 2011. Protective actions of green tea polyphenols and alfacalcidol on bone microstructure in female rats with chronic inflammation. Journal of Nutritional Biochemistry. 22(7):673-680.Interpretive Summary: Chronic inflammation is associated with bone loss and bone structure deterioration. Agents, such as green tea polyphenols and vitamin D possess anti-oxidant and/or anti-inflammatory property and have been shown to protect animals from bone loss due to chronic inflammation.
In present study, we evaluated whether green tea polyphenols (green tea bioactive components) in combination with vitamin D can mitigate bone loss in female rats with chronic inflammation induced by lipopolysaccharide implantation. We found that lipopolysaccharide implantation decreased trabecular volume, thickness, and number in proximal tibia and femur. Supplementation of green tea polyphenols and vitamin D reversed lipopolysaccharide-induced detrimental changes in bone. Both green tea polyphenols and vitamin D improved femoral strength and suppressed TNF-alpha expression in proximal tibia.  We conclude that green tea polyphenols and vitamin D are beneficial to bone health.
                                Technical Abstract: This study investigated the effects of green tea polyphenols (GTP) and alfacalcidol on bone microstructure and strength along with possible mechanisms in rats with chronic inflammation. A 12-week study using a 2 (no GTP vs. 0.5%, w/v GTP in drinking water) × 2 (no alfacalcidol vs. 0.05 ug/kg alfacalcidol orally, 5x/week) factorial design was employed in lipopolysaccharide (LPS)-administered female rats. A group receiving placebo administration was used to compare with a group receiving LPS administration only to evaluate the effect of LPS. Changes in tibial and femoral microarchitecture, and strength of femur were evaluated. Difference in expression of tumor necrosis factor-alpha'(TNF-alpha) in proximal tibia using immunohistochemistry was examined. Compared to the placebo group, the LPS-administered only group had significantly lower femoral mass, trabecular volume, thickness, and number in proximal tibia and femur, and lower periosteal bone formation rate in tibial shafts, while had significantly higher trabecular separation and osteoclast number in proximal tibia, and eroded surface in endocortical tibial shafts. Both GTP and alfacalcidol reversed these LPS-induced detrimental changes in femur, proximal tibia, and endocortical tibial shaft. Both GTP and alfacalcidol also significantly improved femoral strength, while significantly suppressed TNF-alpha expression in proximal tibia. There were significant interactions in femoral mass and strength, trabecular separation, osteoclast number, and TNF-alpha'expression in proximal tibia. A combination of both showed to sustain bone microarchitecture and strength. We conclude that a protective impact of GTP and alfacalcidol in bone microarchitecture during chronic inflammation may be due to a suppression of TNF-alpha.


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