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首页> 外文期刊>The Journal of Nutritional Biochemistry >Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model.
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Green tea polyphenols mitigate bone loss of female rats in a chronic inflammation-induced bone loss model.

机译:在慢性炎症诱导的骨质流失模型中,绿茶多酚可减轻雌性大鼠的骨质流失。

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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)]x2 (no GTP vs. 0.5% GTP in drinking water) factorial design enabled the evaluation of effects of LPS administration, GTP levels, and LPSxGTP 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- alpha (TNF- alpha) 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- alpha 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- alpha 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.
机译:这项研究的目的是探讨与预防慢性炎症大鼠骨丢失有关的绿茶多酚(GTP)的生物利用度,功效和分子机制。 2 [安慰剂与脂多糖(LPS)] x2(无GTP与饮用水中0.5%GTP相比)的析因设计可以评估LPS给药,GTP水平和LPSxGTP相互作用的影响。通过高压液相色谱法分别测定了尿液中的GTP成分和8-羟基-2'-脱氧鸟苷(8-OHdG)的生物利用度和分子机理。通过使用双能X射线吸收法检查股骨矿物质含量(BMC)和密度(BMD)的变化以及使用相应的ELISA试剂盒检查骨转换生物标志物[骨钙蛋白(OC)和抗酒石酸的酸性磷酸酶(TRAP)]来评估疗效。 。通过实时RT-PCR测定脾脏中肿瘤坏死因子-α(TNF-α)和环氧合酶-2(COX-2)的mRNA表达。在整个研究期间,LPS给药和GTP水平均不会影响体重和股骨面积。仅补充GTP会导致尿中表没食子儿茶素和表儿茶素的浓度增加。 LPS给药导致股骨BMC和BMD降低以及血清OC水平降低,但血清TRAP,尿中的8-OHdG和脾脏mRNATNF-α和COX-2表达增加。 GTP补充导致股骨BMC,BMD和血清OC值升高,但血清TRAP,尿中的8-OHdG和脾脏mRNATNF-α和COX-2表达降低。我们得出结论,GTP通过减少氧化应激诱导的损伤和炎症减轻了慢性炎症诱导的骨丢失模型中的骨丢失。

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