Osteoporosis is a major health problem in postmenopausal women globally. This study determined the mechanism through which coelogin stimulates osteoblastogenesis and its osteoprotective and bone regenerating potential. Coelogin effect on primary calvarial osteoblast cells was determined by measuring alkaline phosphatase activity, mineralization, osteoblast survival, and apoptosis and protein expression studies. The osteoprotective effect of coelogin was also evaluated on osteopenic adult female Swiss mice. At autopsy, bones were collected for dynamic and histomorphometry studies. Serum samples were also collected for assessment of serum parameters. Coelogin treatment led to increased osteoblast proliferation, survival, differentiation, and mineralization in osteoblast cells. Coelogin supplementation to Ovx mice promoted new bone formation, prevented Ovx-induced deterioration of bone microarchitecture, and enhanced bone regeneration. In addition, signaling studies revealed that coelogin treatment activates the ER-Erk and Akt-dependent signaling pathways which stimulate the osteoblastogenesis in osteoblast cells.

骨质疏松症是全球绝经后妇女的主要健康问题。这项研究确定了腔肠素刺激成骨细胞生成的机制及其骨保护和骨再生潜力。通过测量碱性磷酸酶活性、矿化、成骨细胞存活以及细胞凋亡和蛋白质表达研究来确定腔肠素对原代颅骨成骨细胞的影响。腔肠素对骨质减少的成年雌性瑞士小鼠的骨保护作用也进行了评估。在尸检时，收集骨骼用于动态和组织形态学研究。还收集血清样品用于评估血清参数。Coelogin 治疗导致成骨细胞增殖、存活、分化和矿化增加。向 Ovx 小鼠补充 Coelogin 促进新骨形成，防止 Ovx 引起的骨微结构恶化，并增强骨再生。此外，信号研究表明腔肠素治疗会激活 ER-Erk 和 Akt 依赖性信号通路，这些通路刺激成骨细胞中的成骨细胞生成。