续断皂苷Ⅵ对小鼠骨髓基质干细胞成骨分化的影响

Effect of Asperosaponin Ⅵ on osteogenic differentiation of bone marrow stromal cells and anti-osteoporosis in mice

目的:探讨续断皂苷VI(ASA VI)对小鼠骨髓基质干细胞(BMSCs)成骨分化的作用机制及对小鼠骨质疏松的防治作用。方法:采用MTT法、钙浓度检测及RT-q PCR方法评价ASA VI对BMSCs细胞活力、成骨分化及Wnt通路相关基因表达的作用;通过Micro-CT定量分析ASA VI对去卵巢(OVX)小鼠骨形态计量参数的影响。结果:适宜浓度下的ASA VI能提高BMSCs的细胞活力,促进细胞基质矿化,升高BMP-2、Runx2、β-catenin、OCN的基因表达,Wnt信号阻断剂(DKK-1)能降低这些成骨基因表达。ASA VI能增加OVX小鼠的股骨骨量,改善骨小梁微结构。结论:ASA VI促进BMSCs成骨分化,Wnt信号可参与了ASA VI诱导的成骨分化过程。

Objective： To investigate the underlying mechanisms of Asperosaponin VI （ASA VI） on bone marrow stromal cells （BMSCs） and the osteoprotective effect of ASA VI in mice after an ovariectomy （OVX）. Methods： The effect of ASA VI at various concentrations on BMSCs proliferation, differentiation and express of mRNAs related to Wnt signal were measured with the MTT assay, calcium deposition assay and quantitative-RT-PCR, respectively. Micro-CT was employed for scanning the microstructural indices of the mice after an ovariectomy （OVX）. Results： ASA VI at the appro-priate concentration enhanced the BMSCs proliferation, mineralization and osteogenic gene expression, including BMP- 2, Runx2, β-catenin, OCN. ASA VI-induced gene expression levels were significantly reduced by pretreatment with DKK- I. Moreover, ASA VI preserved the trabecular bone microarchitecture of OVX mice in vivo. Conclusion： ASA VI induced the BMSCs osteogenic differentiation by activating the Wnt/β-catenin pathway.