目的　探讨辛伐他汀（simvastatin,SIM）是否可以通过调节TGF-β1/Smad通路从而促进大鼠骨髓间充质干细胞(bone marrow mesenchymal stem cells , BMSCs)分化为成骨样细胞。　方法　复苏、培养大鼠BMSCs并诱导其向成骨样细胞分化。实验组加入不同浓度的SIM（10-8 mol/L、10-7 mol/L、10-6 mol/L），对照组不给予药物干预。加入成骨诱导液，7d后运用碱性磷酸酶染色法观察细胞成骨能力，21d后用茜素红染色检测细胞钙化水平，Western blot法检测TGF-β1、Smad2、Smad3蛋白的表达水平。  结果　应用10-8 mol/L～10-6 mol/L SIM处理细胞7d均可使细胞ALP活性显著增加，其中浓度为10-7 mol/L时效果最显著；应用10-8 mol/L～10-6mol/L SIM处理细胞21d后可使细胞钙化结节明显增多；应用10-8 mol/L～10-6 mol/L SIM处理细胞7d后细胞内TGF-β1、Smad2、Smad3蛋白水平明显增高。 结论　辛伐他汀可促进大鼠BMSCs分化为成骨细胞，其作用机制可能与上调TGF-β1/Smad信号通路中相关基因的表达水平有关。

Objective    To investigate whether simvastatin(SIM) can promote differentiation of rat bone marrow mesenchymal stem cells(BMSCs ) to osteablasts by regulating TGF-β1/Smad signaling pathways.  Methods   Rat BMSCs were recovered, cultured and further induced to differentiate into osteoblasts. Different concentration of SIM（10-8 mol/L、10-7 mol/L、10-6 mol/L） was added in the experimental group, and the control group no drug intervention was given in the control group. 7 days after ostrogenic solution was added, alkaline phosphatase staining was used to observe the expression level of bone formation, Alizarin Red staining was used to observe calcification level,and Western blot was used to determine the expression of of TGF-β1,Smad2 and Smad3.   Results   Treatment with SIM at concentrations of 10-8 mol/L to 10-6 mol/L for 7 d  significantly increased the activity of ALP, and SIM at concentration of 10-7 mol/L produced the maximum effect. Exposure of the cells to SIM at concentration of 10-8 mol/L～10-6 mol/L for 21 d significantly increased mineralized nodules. Exposure of the cells to SIM at concentrations of 10-8～10-6 mol/L for 7 d markedly increased the expression of TGF-β1, Smad2 and Smad3.   Conclusion   SIM could promote the osteogenic differentiation of BMSCs，in which process the changes of the mRNA expression levels inTGF-β1/Smad signaling pathway might participate.