本实验发现OVX+OC组中破骨细胞出现最早，个数最多，凋亡时间最晚，OVXDF+OC组次之，SHAM+OC组最低。表明在存在破骨细胞诱导剂的情况下，与正常大鼠BMSCs相比，绝经后大鼠BMSCs对破骨细胞分化成熟的抑制作用减弱，而经骨碎补灌胃后的绝经后大鼠BMSCs对破骨细胞的分化成熟的抑制作用得到加强，显示骨碎补可以通过BMSCs来抑制破骨细胞的分化及成熟。共培养系统中上清液以及BMSCs内，RANKL RANKL/OPG：SHAM+OC组OVXDF+OC组>OVX+OC组，表明绝经后骨质疏松大鼠BMSCs内及其分泌的OPG降低，而RANKL升高，RANKL/OPG比例升高，从而激活OPG/RANKL/RANK信号通路促进破骨细胞的分化、成熟。经骨碎补灌胃后，OPG升高，RANKL降低，RANKL/OPG比例降低，抑制OPG/RANKL/RANK信号通路，抑制破骨细胞的分化、成熟。同时，灌胃后大鼠BMSCs中Wnt10b及β-catenin mRAN及蛋白含量升高，提示在此过程中骨碎补同时激活了Wnt/β-catenin信号通路。虽然具体作用机制尚不明确[29]，但众多研究表明Wnt/β-catenin通路的激活可升高OPG，降低RNAL[30-31]，因此，推测骨碎补调节BMSCs OPG及RANKL可能与Wnt/β-catenin通路的激活有关。由于OPG、RANKL的分泌受多种机制调控，实验过程中OPG、RANKL的变化是否仅仅由Wnt/β-catenin信号通路的激活引起，是否有其他机制协同作用，尚不明确，还需一步研究。

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