随着人口老龄化，骨质疏松的发病率越来越高，已成为严峻的公共卫生及社会问题。由于现有抗骨质疏松药物的局限性及副作用，应用中医药开展抗骨质疏松治疗已使我国骨质疏松症研究在国际学术界独树一帜。前期研究表明古方青娥丸对绝经后骨质疏松患者有明确的治疗作用，其疗效机理之一与该方能调控Wnt/β-catenin信号通路抑制因子Sclerostin及RANKL/OPG蛋白水平有关。近年来研究发现，BMP-Smads信号通路关键分子BMPRIa能上调sclerostin及RANKL/OPG调控的破骨细胞形成，进而抑制Wnt经典信号通路，降低骨量。为探讨青娥丸对BMP-Smads信号通路的影响，我们运用青娥丸干预去卵巢骨质疏松小鼠模型及成骨细胞、破骨细胞，检测骨标志物及BMP-Smads信号通路因子水平以期阐明骨质疏松发病机理和治疗靶点，揭示青娥丸是否通过调节BMP-Smads信号通路达到治疗骨质疏松的作用。

As the population ages, the incidence of osteoporosis is higher and higher. It has become a serious public health and social problems. Because of the limitations and side effects of existing anti-osteoporosis drug, application of Chinese medicine in anti-osteoporosis treatment is unique in China also in the international academia. Early research has shown that ancient formula Qing'E has definite therapeutic effect in patients with postmenopausal osteoporosis. One of the mechanisms of curative effect is that it can regulate Sclerostin, the Wnt/β- catenin signaling pathway inhibitor, and RANKL/OPG proteins levels. Recent studies have found that the key molecular BMPRIa in BMP/Smads signaling pathways can upregulate Sclerostin level and osteoclast formation regulated by RANKL/OPG, thereby inhibit classic Wnt signaling pathway and reduce bone mass. In order to further clarify the relationship between BMP-Smads signaling pathway and osteoporosis, at the same time to explore the effect of ancient formula Qing'E on BMP-Smads signaling pathway, we use Qing'E to intervent ovariectomized osteoporosis mice model and osteoblasts and osteoclasts, then detect bone metabolic markers and partial factor levels in BMP-Smads signaling pathways. Ultimately we clarify the pathogenesis of osteoporosis and treatment targets and reveal whether Qing'E treat osteoporosis by mediating the BMP-Smads signaling pathway.