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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 mechanism of action of saponin VI (ASA VI) on osteogenic differentiation of mouse bone marrow stromal stem cells (BMSCs) and its preventive and therapeutic effects on mice osteoporosis. Methods: The effects of ASA VI on the viability, osteogenic differentiation and Wnt pathway-related gene expression of BMSCs were evaluated by MTT assay, calcium concentration assay and RT-q PCR method. The effect of ASA VI on the ovariectomized (OVX) Effect of rat bone morphometric parameters. RESULTS: ASA VI at appropriate concentration increased the viability of BMSCs, promoted the matrix mineralization and increased the gene expression of BMP-2, Runx2, β-catenin and OCN. Wnt signaling inhibitor (DKK-1) These osteogenic genes are expressed. ASA VI increased femoral bone mass in OVX mice and improved trabecular bone microstructure. CONCLUSION: ASA VI promotes osteogenic differentiation of BMSCs. Wnt signaling is involved in ASA-induced osteogenic differentiation.