糖皮质激素（GC）性骨质疏松症（GIO）是GC最严重的副作用之一。骨形成抑制是其发生的关键，但目前的药物多针对骨吸收，针对骨形成的较少。我们前期研究发现：五味子丙素（SC）能够拮抗地塞米松（Dex）诱导的成骨细胞增殖抑制及小鼠胫骨皮质厚度、骨量及密度下降，并能拮抗Dex对CyclinD1表达和ERK、AKT磷酸化的抑制，提示其可能能够通过调控这些通路促进骨形成抗GIO。然而，在吸附掉血清中的细胞因子后，SC拮抗Dex对成骨细胞增殖抑制的作用消失了，提示SC不是直接作用于上述信号通路，而可能是通过调节细胞膜受体、放大/抑制原有的配体/受体信号传导，进而影响胞内信号转导发挥促进骨形成作用的。受体酪氨酸激酶（RTK）是胞外信号向胞内传导的重要受体，可调控上述通路促进骨形成。因此，我们拟从RTK中筛选SC的作用靶点，探讨SC对RTK介导的信号通路的调控，初步阐明SC促进骨形成防治GIO的作用机制。

Glucocorticoid (GC)-induced osteoporosis (GIO) is one of the most serious side effects of GC. Inhibition of bone formation is the key mechanism of GIO. However, most drugs for GIO target bone resorption currently. Our previous study found that schisandrin C (SC) was able to antagonize dexamethasone (DEX)-induced inhibition of osteoblasts proliferation and decrease of thickness, bone mass and density of mouse Tibial cortex, suggesting that it may exert anti-GIO effect through promoting bone formation. SC could also antagonize the effect of Dex on the expression of CyclinD1 and phosphorylation of ERK and AKT, suggesting that its mechanism may be related to the regulation of these pathways. However, after removing the cytokines in serum with acticarbon, the antagonism effect of SC on DEX-induced osteoblasts proliferation inhibition disappeared, indicating that the above pathways are not the direct target of SC, and SC may exert promoting the formation of bone by regulating the cell membrane receptor, then amplifying/inhibiting the original ligand/receptor mediated signaling. Receptor tyrosine kinases (RTKs) are important receptors for the transduction of extracellular signals and closely relate with bone formation. Therefore, we intend to investigate the effect and mechanism of SC on bone formation and GIO through regulating RTKs-mediated signal pathway.