中文摘要：

氧化应力，煽动性的反应，和激活 mitogen 的蛋白质 kinases (MAPK ) 串联是骨质疏松症的重要病原的因素。提高的 homocysteine (Hcy ) 可以在绝经后的骨质疏松症激活氧化应力和还原剂骨头矿物质密度，这被报导了。而且，荷尔蒙代替治疗广泛地在诊所被使用了与骨质疏松症阻止并且对待绝经后的女人， osteoporotic 骨折和位于 Hcy 的行动下面的相关信号 transduction 小径仍然保持不清楚。在这研究，我们调查了 17-estradiol 的效果(导致 Hcy 的氧化压力，煽动性的反应和 MAPK 串联，以及内在的信号 transduction 小径在上的 17-E ₂) 鼠科未加工 264.7 个房间。反应的氧种类(ROS ) 被 fluorospectrophotometry 估计。proinflammatory cytokines 肿瘤坏死因素 --(TNF-) 并且 interleukin (IL )-1 被 double-immunofluorescence 标记和反向的 transcriptase 聚合酶链反应试金分析分别地。而且， MAPK 串联的 phosphorylation 层次被西方的污点分析测量。一个特定的 phosphatidylinositol 3-kinase (PI3-K ) 禁止者， Wortmannin (1 M ) 被采用决定 PI3-K/Akt 发信号小径是否调停了 17-E ₂ 的效果在上未加工 264.7 个房间。17-E ₂ 显著地减少了 ROS 生产由 Hcy 导致了，在蛋白质和 mRNA 的 TNF-1 和 IL-1 的表示铺平，并且下面调整 MAPK (ERK1/2， JNK 和 p38 ) 的 phosphorylation。导致 Hcy 的变化上的 17-E ₂ 的这些压制的效果被预告的处理与 PI3-K 禁止者 Wortmannin 颠倒。结果显示那 17-estradiol 可以稀释 MAPK 的导致 Hcy 的氧化应力，煽动性的反应和起来规定在未加工经由 PI3-K/Akt 的 264.7 个房间表明 transduction 小径。

英文摘要：

Oxidative stress, inflammatory response, and mitogen-activated protein kinases （MAPKs） cascade are significant pathogenic factors of osteoporosis. It has been reported that elevated homocysteine （Hcy） may activate oxidative stress and reduce bone mineral density in post-menopausal osteopor- osis. Moreover, hormone replacement therapy has been widely used in clinic to prevent and treat post-menopausal women with osteoporosis and osteoporotic fracture, but the molecular mechan- isms and relevant signal transduction pathways underlying the action of Hcy remain unclear. In this study, we investigated the effects of 17β-estradiol （17β-E2） on the Hcy-induced oxidative stress, inflammatory response and MAPKs cascade, as well as the underlying signal transduction pathway in murine Raw 264.7 cells. The reactive oxygen species （ROS） was assessed by fluorospectrophoto- metry. The proinflammatory cytokines tumor necrosis factor-α （TNF-α） and interleukin （IL）-1β were analyzed by double-immunofluorescence labeling and reverse transcriptase polymerase chain reac- tion assay, respectively. Furthermore, phosphorylation levels of MAPKs cascade were measured by western blot analysis. A specific phosphatidylinositol 3-kinase （PI3-K） inhibitor, Wortmannin （1 μM） was employed to determine whether PI3-K/Akt signaling pathway mediated the 17β-E2＇s effect on Raw 264.7 cells. 171β-E2 markedly decreased the ROS production induced by Hcy, the expression of TNF-α and IL-1β at protein and mRNA levels, and down-regulated the phosphorylation of MAPKs （ERK1/2, JNK and p38）. These suppressing effects of 17β-E2 on Hcy-induced changes were reversed by pretreatment with PI3-K inhibitor Wortmannin. The results indicate that 17β-estradiol may attenu- ate Hcy-induced oxidative stress, inflammatory response and up-regulation of MAPKs in Raw 264.7 cells via PI3-K/Akt signal transduction pathway.