Department of Pathology, Texas Tech University Health Sciences Center, Lubbock, TX 79430-9097, USA.
J Nutr Biochem. 2010 Oct;21(10):968-74. doi: 10.1016/j.jnutbio.2009.08.002. Epub 2009 Dec 4.
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)]×2 (no GTP vs. 0.5% GTP in drinking water) factorial design enabled the evaluation of effects of LPS administration, GTP levels, and LPS×GTP 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-α (TNF-α) 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-α 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-α 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.
本研究旨在探讨绿茶多酚（GTP）在预防慢性炎症大鼠骨丢失中的生物利用度、疗效和分子机制。采用 2 [安慰剂与脂多糖（LPS）]×2（饮用水中无 GTP 与 0.5% GTP）析因设计，评估 LPS 给药、GTP 水平和 LPS×GTP 相互作用的影响。通过高压液相色谱法测定尿 GTP 成分和 8-羟基-2'-脱氧鸟苷（8-OHdG）水平，分别评估生物利用度和分子机制。采用双能 X 射线吸收法测定股骨矿物质含量（BMC）和密度（BMD）的变化来评估疗效，并采用各自的 ELISA 试剂盒测定骨转换生物标志物[骨钙素（OC）和抗酒石酸酸性磷酸酶 5b（TRAP）]。实时 RT-PCR 测定脾组织肿瘤坏死因子-α（TNF-α）和环氧化酶-2（COX-2）的 mRNA 表达。在整个研究期间，LPS 给药或 GTP 水平均不影响体重和股骨骨面积。只有 GTP 补充可增加尿表没食子儿茶素和表儿茶素浓度。LPS 给药导致股骨 BMC 和 BMD 以及血清 OC 水平降低，但血清 TRAP、尿 8-OHdG 和脾 TNF-α 和 COX-2 mRNA 表达水平升高。GTP 补充可使股骨 BMC、BMD 和血清 OC 升高，而血清 TRAP、尿 8-OHdG 和脾 TNF-α 和 COX-2 mRNA 表达水平降低。我们得出结论，GTP 通过减少氧化应激诱导的损伤和炎症来减轻慢性炎症诱导的骨丢失模型中的骨丢失。
