骨质疏松症主要由于成骨细胞骨形成和破骨细胞骨吸收平衡失调所致。细胞自噬即能影响成骨细胞增殖与活性又能影响破骨细胞的活性和功能。本项目以明确mTORCl在骨质疏松模型大鼠椎体、OB、OC培养体系、OB与OC共育体系中对细胞自噬与凋亡调节机制为切入点，在骨质疏松大鼠模型上给予慢病毒和补肾益髓中药骨乐冲剂进行干预，在三种细胞模型上给予慢病毒和中药血清进行干预，使用电子显微镜观察细胞自噬与凋亡情况，通过Real-time PCR与Western blot在分子水平检测OB、OC自噬与凋亡相互调节关键基因mTORCl表达变化，同时观察反应细胞自噬与凋亡的AKT、ATG、VPS9、BCL-XL、BCL-2、BAX、mTORC1、 Caspase-3、LC3-Ⅱ/Ⅰ等主要指标及其蛋白表达变化，在分子水平阐明mTOＲ信号通路对骨质疏松症发病动态平衡中细胞自噬与凋亡相互调节的影响及补肾益髓中药的作用机理。

There are two specific cells responsible for the maintenance of constant bone mass: osteoblasts (OB bone-forming cells), and osteoclasts (OC bone resorbing cells). The proper balance between these two opposing processes is essential for bone health, and disruption of this balance favoring resorption causes osteopenia and eventually osteoporosis. Autophagy, a physiological process involved in the regulation of cells, control the generation and activity of osteobalsts and osteoclasts. To identify cell autophagy and apoptosis regulation mechanism, we used osteoporosis rats treated with lentivirus and GuLe, three kingds of cell models treated with lentivirus and serum of traditional Chinese medicine. MTORC1, the key gene target of osteocyte autophagy and apoptosis was detected respectively by Transmission Electron Microscopy (TEM), realtime-PCR and Western blot. In addition, AKT、ATG、VPS9、BCL-XL、BCL-2、BAX、mTORC1、Caspase-3 and LC3-Ⅱ/Ⅰwere analyzed. The purpose of this study was to clarify the mechanism of mTOR signal pathway in the pathogenesis of osteoporosis and the interaction between autophagy and apoptosis is associated with herbs of invigorating kidney and benefiting marrow.