Department of Pathology, Texas Tech University Health Sciences Center, BB 198, 3601 4th Street, Lubbock, TX 79430-9097, USA.
Osteoporos Int. 2011 Jan;22(1):327-37. doi: 10.1007/s00198-010-1209-2. Epub 2010 Mar 20.
Green tea polyphenols (GTP) are promising agents for preventing bone loss. GTP supplementation sustained microarchitecture and improved bone quality via a decrease in inflammation. Findings suggest a significant role for GTP in skeletal health of patients with chronic inflammation.
This study evaluated whether GTP can restore bone microstructure along with a molecular mechanism in rats with chronic inflammation. A 2 [placebo vs. lipopolysaccharide (LPS)]× 2 [no GTP vs. 0.5% GTP (w/v) in drinking water] factorial design was employed.
Female rats were assigned to four groups: placebo, LPS, placebo + GTP, and LPS + GTP for 12 weeks. Efficacy was evaluated by examining changes in bone microarchitecture using histomorphometric and microcomputed tomographic analyses and by bone strength using the three-point bending test. A possible mechanism was studied by assessing the difference in tumor necrosis factor-α (TNF-α) expression in tibia using immunohistochemistry.
LPS lowered trabecular volume fraction, thickness, and bone formation in proximal tibia while increasing osteoclast number and surface perimeter in proximal tibia and eroded surface in endocortical tibial shafts. GTP increased trabecular volume fraction and number in both femur and tibia and periosteal bone formation rate in tibial shafts while decreasing trabecular separation in proximal tibia and eroded surface in endocortical tibial shafts. There was an interaction between LPS and GTP in trabecular number, separation, bone formation, and osteoclast number in proximal tibia, and trabecular thickness and number in femur. GTP improved the strength of femur, while suppressing TNF-α expression in tibia.
In conclusion, GTP supplementation mitigated deterioration of bone microarchitecture and improved bone integrity in rats with chronic inflammation by suppressing bone erosion and modulating cancellous and endocortical bone compartments, resulting in a larger net bone volume. Such a protective role of GTP may be due to a suppression of TNF-α.
本研究旨在评估绿茶多酚（GTP）是否可以恢复慢性炎症大鼠的骨微结构及其分子机制。采用 2 [安慰剂对照 vs. 脂多糖（LPS）]×2 [无 GTP 对照 vs. 饮用水中 0.5% GTP（w/v）]析因设计。
将雌性大鼠分为 4 组：安慰剂、LPS、安慰剂+GTP 和 LPS+GTP，共 12 周。通过组织形态计量学和 microCT 分析评估骨微结构变化，通过三点弯曲试验评估骨强度，通过免疫组化评估胫骨中肿瘤坏死因子-α（TNF-α）表达的差异来研究可能的机制。
LPS 降低了胫骨近端的小梁体积分数、厚度和骨形成，同时增加了胫骨近端的破骨细胞数量和表面周长以及皮质内胫骨的侵蚀表面。GTP 增加了股骨和胫骨的小梁体积分数和数量，以及胫骨骨干的骨形成率，同时降低了胫骨近端的小梁分离和皮质内胫骨的侵蚀表面。LPS 和 GTP 之间存在交互作用，影响了胫骨近端的小梁数量、分离、骨形成和破骨细胞数量，以及股骨的小梁厚度和数量。GTP 改善了股骨的强度，同时抑制了胫骨中 TNF-α 的表达。
总之，GTP 补充通过抑制骨侵蚀和调节松质骨和皮质骨腔室，改善了慢性炎症大鼠的骨微结构和完整性，导致净骨体积增加。GTP 的这种保护作用可能是由于 TNF-α 的抑制。
