DHEA对间充质干细胞分化为成骨细胞及其成骨作用的调节机制

绝经后骨质疏松症（PMO）是绝经后女性常见的骨代谢疾病，其发生机制是成骨细胞和破骨细胞引起的机体骨重建失衡，其中，成骨细胞的生成及功能起关键作用。绝经后骨质疏松症最普遍的治疗方法是雌激素替代治疗（ERT），其原理主要是作用于破骨细胞引起的骨吸收，而作用于骨形成方面的研究甚少。DHEA对成骨细胞的调节作用已有相关研究，但对于成骨细胞形成方面的研究甚少。课题组前期研究发现，间充质干细胞(MSCs)可以分化为成骨细胞，亦可以分化为脂肪细胞，MSCs不能优势分化为成骨细胞可能引起骨质疏松症。本课题以间充质干细胞为研究对象，通过与骨髓单核细胞共培养，研究DHEA对成骨细胞形成及其成骨作用的调节，并分析DHEA发挥调节作用的机制。本课题从成骨细胞形成方面研究PMO防治，将推进PMO防治新策略的产生，同时也将促进围绝经期内分泌代谢网络理论向纵深发展。

Postmenopausal osteoporosis (PMO) is a metabolic bone disease always happened in postmenopausal women，which mechanism is the imbalance of bone reboding induced by osteoblast and osteoclast,and that osteoblast formation and function is the most important. The most comman theraputic method of PMO is estrogen replacement therapy(ERT),which is acting on the bone absorption by osteoclast ,but there is little methods acting on bone formation.DHEA can regulate osteoblast proliferation,but study on regulating osteoblast formation is few.In our study,mesenchymal stem cells (MSCs)can differentiate into osteobalsts and adipocytes,and the decreased numbers of osteoblasts maybe an important reason of osteoporosis.In this study,we use the co-culture system of MSCs and BMMs to investigate the regulating mechanisms of DHEA on MSCs differentiation into osteoblast and osteoblast function ,which will promote the theraputic methods of PMO,and the development of menopausal period secretion metabolic network theory.