淫羊藿次苷II是中医治疗骨质疏松症的常用中药淫羊藿在体内的主要代谢产物之一，具有抗骨质疏松作用，但药效及具体机制不明确。我们已证明：钙结合蛋白S100A16抑制骨髓间充质干细胞（BMSCs）成骨分化促进其成脂分化。我们还发现：淫羊藿次苷II能够 ①比淫羊藿更有效地改善小鼠骨质疏松；②强烈下调S100A16蛋白表达；③诱导BMSCs成骨分化，高表达S100A16削弱这一作用；④激活Wnt/β-Catenin通路，抑制此通路削弱淫羊藿次苷II对S100A16的下调作用。由此，我们推测：淫羊藿次苷II通过抑制S100A16促进BMSCs成骨分化抑制其成脂分化进而发挥抗骨质疏松作用。本研究拟通过骨质疏松小鼠模型和原代细胞模型，结合CT、成骨成脂分化、报告基因分析等手段对此假说进行验证。本项目的研究结果将揭示淫羊藿治疗骨质疏松的有效成分及其分子机制，为中药治疗骨质疏松的全球性推广提供理论和实验研究。

Icariside II is the main active metabolite of icariin which has the function of suppressing osteoporosis, but the molecular mechanism remains unclear. In our previous studies, we have demonstrated that S100A16 was able to promote the differentiation of bone marrow mesenchymal stem cells (BMSCs) into lipocytes instead of osteoblast. Our recent data showed that ① icariside II improved osteoporosis effectively compared with icariin; ② icariside II markedly downregulated the expression of S100A16; ③ overexpression of SA00A16 impaired the promoting osteoblastic differentiation of BMSCs induced by icariside II; ④ Wnt/β-catenin signalling pathway was activated by icariside II and inhibition of this pathway attenuated the downregulation of S100A16 caused by icariside II. Therefore, we postulate that icariside II may promote the osteogenic differentiation of BMSCs and inhibit the adipogenic differentiation by downregulation of the expression of S100A16, which is caused by the activation of Wnt/β-catenin signaling pathway. We will test this hypothesis by construction of the osteoporosis mouse model and separation of primary cells, as well as combination with microCT and luciferase reporter assays, etc. Results of this project will reveal the roles and molecular mechanisms of icariside II in suppression of osteoporosis,thus provide the theoretical and experimental basis for the popularization of treatment of osteoporosis using traditional Chinese medicine.