类风湿关节炎（RA）主要的致残原因是滑膜炎、血管翳形成后造成的关节骨质破坏，延缓甚至阻断骨质破坏成为RA治疗的重要目标之一。破骨细胞是RA关节软骨和骨质破坏的重要参与者，OPG-RANKL-RANK是调节破骨细胞分化和成熟最重要的信号通路。探索其调控机制，有助于寻找干预RA骨破坏的作用靶点。桂枝芍药知母汤是临床上治疗RA的经典方剂，临床疗效显著。基于以上开展下列研究：（1）在体研究：复制胶原诱导性关节炎（CIA）大鼠模型后，以桂枝芍药知母汤为干预手段，观察关节组织形态学、影像学变化，OPG-RANKL-RANK信号通路、细胞因子及淋巴细胞增殖情况；（2）体外研究：以RAW264.7细胞建立破骨细胞分化模型，桂枝芍药知母汤含药血清干预后，研究其细胞形态、细胞增殖能力、骨吸收能力及细胞因子变化。目的：从骨免疫学角度，研究桂枝芍药知母汤通过OPG-RANKL-RANK信号通路对RA的调控机制。

The main causes of disability caused by Rheumatoid arthritis （RA）are synovial inflammation and joint bone destruction caused after pannus formation, thus delaying or even blocking bone destruction became one of the important goals of RA therapy. Osteoclast is an important participant in the process of RA joint cartilage and bone destruction, and OPG-RANKL-RANK is one of the most important signaling pathways in the regulation of osteoclast differentiation and maturation. To explore the regulation mechanism of it will be helpful to find the intervention target of RA bone destruction. Guizhi Shaoyao Zhimu Decoction（GSZD）, a classic prescription, is used for the treatment of RA clinically, which has good clinical curative effect. In this study, these works will be done as followed： （1）duplicating induced collagen induced arthritis（CIA）rat model and treated with GSZD, and the changes of morphology, imageology, OPG-RANKL-RANK signaling pathway, cytokines and lymphocyte proliferation will be observed. （2）RAW264.7 cells will be used to induce osteoclast differentiation model, and intervened by GSZD. The changes of cell morphology, cell proliferation capacity , bone absorbing capacity and supernatant cytokine changes will be explored .Purpose to explore the regulation mechanism of Guizhi Shaoyao Zhimu Decoction for rheumatoid arthritis by OPG-RANKL-RANK signaling pathways based on Osteoimmunology.