青蒿素联合PACER通过RANK/RANKL/NF-κB通路抑制破骨细胞活化作用及其机制研究

我们提出的科学问题是，青蒿素及PACER在破骨细胞形成及功能活化中的调控作用如何，两者的调控基因和信号传导通路是否均与RANK/RANKL/.NF-κB通路相关？通过前期研究发现，青蒿素呈剂量依赖性地抑制破骨细胞的形成以及延缓破骨细胞所致骨溶解，其机制与抑制NF-κB通路有关。本实验将从体内外观察青蒿素、PACER对破骨细胞分化及功能活化的影响，鉴定两者的调控作用，分析相关调控机制与RANK/RANKL/NF-κB.信号通路的关系，从而阐明青蒿素、PACER调控破骨细胞分化及功能活化的分子机制，为治疗过度破骨细胞性骨吸收疾病提供新的治疗思路——青蒿素与抑制PACER联合，共同减少机体破骨细胞形成及抑制其功能活化，从而治疗过度破骨细胞性骨吸收疾病。

The scientific question we propose is the regulation of artemisinin and PACER in the process of osteoclast formation and function activation, whether the regulatory genes and signal transduction pathways are related to RANK/RANKL/NF- kappa B pathway related? The preliminary study found that artemisinin was dose dependently inhibited the formation of osteoclasts and osteoclast induced delayed osteolysis, and its mechanism is related to inhibition of NF- kappaB pathway. This experiment will be observed from the in vivo effects of artemisinin, activation of PACER on differentiation and function of osteoclasts, regulation of the identification, analysis of the relationship between the regulatory mechanism of RANK/RANKL/NF- and B signaling pathway, so as to clarify the molecular mechanism of artemisinin, PACER modulation of osteoclast differentiation and function of bone cell activation, provide treatment of artemisinin and inhibition of PACER combined with new ideas for the treatment of diseases absorption excessive osteoclastic bone, reduce the body to osteoclast formation and inhibition of the activation function, thus the treatment of excessive osteoclastic bone resorption diseases.