Osteoporosis is a reduction in skeletal mass due to the decrease of osteogenic ability and the activation of the osteoclastic function. Inhibiting bone resorption and accelerating the new bone formation is a promising strategy to repair the bone defect of osteoporosis. In this study, we first systematically investigated the roles of Chinese medicine Asperosaponin VI (ASP VI) on osteogenic mineralization of BMSCs and osteoclastogenesis of BMMs, and then explored the synergistic effect of ASP VI and BS (BMP-2 immobilized in 2-N, 6-O-sulfated chitosan) on bone formation. The result showed that ASP VI with the concentration lower than 10⁻⁴ M contributed to the expression of osteogenic gene and inhibited osteoclastic genes RANKL of BMSCs. Simultaneously, ASP VI significantly reduced the differentiation of mononuclear osteoclasts in the process of osteoclast formation induced by M-CSF and RANKL. Furthermore, by stimulating the SMADs, TGF-β1, VEGFA, and OPG/RANKL signaling pathways, ASBS (ASP VI and BS) substantially enhanced osteogenesis, greatly promoted angiogenesis, and suppressed osteoclastogenesis. The findings provide a new perspective on osteoporosis care and prevention.

骨质疏松症是由于成骨能力下降和破骨细胞功能激活而导致的骨骼质量减少。抑制骨吸收和加速新骨形成是修复骨质疏松症骨缺损的一种有前景的策略。在本研究中，我们首先系统地研究了中药天门皂苷 VI（ASP VI）对 BMSCs 成骨矿化和 BMMs 破骨细胞生成的作用，然后探讨了 ASP VI 和 BS（BMP-2 固定在 2-N， 6-O-硫酸化壳聚糖）对骨形成的影响。结果表明，浓度低于 10 ^{-4 的}ASP VI M有助于成骨基因的表达并抑制BMSCs的破骨细胞基因RANKL。同时，在M-CSF和RANKL诱导的破骨细胞形成过程中，ASP VI显着降低了单核破骨细胞的分化。此外，通过刺激 SMADs、TGF-β1、VEGFA 和 OPG/RANKL 信号通路，ASBS（ASP VI 和 BS）显着增强了成骨作用，极大地促进了血管生成，并抑制了破骨细胞生成。这些发现为骨质疏松症的护理和预防提供了新的视角。