我们前期的研究表明肾虚型绝经后骨质疏松症患者成骨细胞的基因及蛋白表达与正常人有明显差异，其中雌激素受体α(ERα)基因及"衰老蛋白"BubR1甲基化异常与绝经后骨质疏松症肾虚的发生有密切关系。甲基化对ERα及BubR1蛋白基因表达调控及其对肾虚型绝经骨质疏松症会产生什么样的遗传学后果，是否影响成骨细胞表型及肾虚的发生与发展，以及传统补肾方药干预后的变化都值得我们更深入的研究。本课题通过MeDIP(甲基化DNA免疫共沉淀)与甲基化芯片结合，检测特定DNA甲基化差异，运用RT-PCR检测甲基化对BubR1蛋白调控的影响，探讨ERα及BubR1蛋白基因甲基化在肾虚型绝经后骨质疏松症发病中的作用机制及其对成骨细胞表型的影响。同时予传统补肾方药干预，研究补肾方药对绝经后骨质疏松症ERα及BubR1启动子甲基化水平及成骨细胞表型的调控机制，探讨中医药治疗肾阳虚及肾阴虚型绝经后骨质疏松症的机理。

Our early research suggests that the biological characteristics of osteoblast in osteoporosis patients are significant different from normal，and the development of nephrasthenia syndrome of osteoporosis is attributable to abnormal methylation of estrogen receptor(ER) gene. And it is valuable to research the effect of epigenetic regulation capacity of ER on the genetic consequences of osteoplast in osteoporosis patients and the osteoblast phenotype. To explore these issues, This subject was aimed at detecting the methylated regions and analyzing the deviation of the DNA methylation, through the application of MeDIP(Methylated DNA coimmunoprecipitation) and Methylation- array by informatics method. Surveying the possibility of effection from the level of methylation of ER gene promoter to the level of methylation of the Genome and the development of nephrasthenia syndrome of osteoporosis, and the transmutation of the level of methylation of CpG island in the target gene of estrogen and osteoblast phenotype, this paper was investigated that the significance and mechanism of the epigenetics of ER Gene methylation to the the development of nephrasthenia syndrome of Osteoporosis.