近期骨免疫学被用于解释绝经后骨质疏松症（PMOP）的发病机理。NF-κB骨免疫通路是PMOP发病的重要途径，但其确切调节机制仍然未知。DANCR是近年来新发现的长链非编码RNA，具有调节NF-κB通路和成、破骨的作用。我们前期芯片检测发现DANCR在PMOP肾阳虚证中显著上调，因此我们假设DANCR调控NF-κB骨免疫通路是PMOP肾阳虚证的重要机制。为证实这一假说，我们应用CRISPR/Cas9、腺病毒沉默和过表达、蛋白悬液芯片等技术来探讨：①DANCR调控NF-κB通路在PMOP肾阳虚证小鼠模型中的骨免疫机制；②在体外，DANCR调控NF-κB骨免疫通路对PMOP肾阳虚证小鼠BMSCs/BMMs成、破骨分化的调节作用；③人血清和椎体骨中，DANCR调控NF-κB骨免疫通路与PMOP肾阳虚证的关联。为挖掘中医药防治PMOP的新靶点及丰富“肾主骨”、“辨证论治”理论的科学内涵提供实验依据。

Osteoimmunology has been well-known introduced in postmenopausl osteoporosis (PMOP). As one of the best important pathway of PMOP, the exact mechanism of NF-κB signaling remains unclear. DANCR, as a long non-coding RNA, plays a critical role in regulation of NF-κB pathway, osteoblastdifferentiation and osteoclast differentiation. Our previous results of gene chip have shown upregulation of DANCR in Kidney-Yang Dificiency of Postmenopausal osteoporosis. Thus we hypothesize that regulation of DANCR on NF-κB osteoimmunology pathway mediates Kidney-Yang Dificiency of Postmenopausal osteoporosis. To verify this hypothesis, three main experiments will be performed through implying CRISPR/Cas9, Adenovirus silence and overexpression,Bio-Plex Assays,etc.Firstly, osteoimmunology mechanism of Kidney-Yang Dificiency of Postmenopausal osteoporosis in mouse will be clarified based on regulation of DANCR on NF-κB pathway. Secondly, the effect of DANCR regulating NF-κB osteoimmunology pathway on osteoblastic/osteoclastic potentials of BMSCs and BMMs, which are from mouse with Kidney-Yang Dificiency of Postmenopausal osteoporosis, will be investigated. Lastly, the correlation between regulation of DANCR on NF-κBosteoimmunology pathway and Kidney-Yang Dificiency of Postmenopausal osteoporosis were demonstrated from human specimen of serum and vertebrae. This study will provide experimental evidence for new therapeutic target of PMOP and theories of “Kidney Dominating Bone”and “Pattern Identification Differentiation and Treatment”.