Tanshinone IIA attenuates osteoclastogenesis in ovariectomized mice by inactivating NF-kB and Akt signaling pathways

American Journal of Translational Research

Shengyuan Zhou¹  Li Cheng² 

[1] Department of Orthopaedics, Cixi Peoples Hospital, Wenzhou Medical University, Cixi 315300, Zhejiang, China;Spine Center, Department of Orthopaedics, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China

关键词: Tanshinone IIA;    postmenopausal osteoporosis;    osteoclastogenesis;    RANK ligand;   

DOI  :  

学科分类：医学（综合）

来源: e-Century Publishing Corporation

【 摘 要 】

Osteoporosis is a common disease associated with age and menopausal status. Postmenopausal osteoporosis is the most common type of primary osteoporosis and is accompanied by increased risk of osteoporotic fracture. Natural and herbal compounds have long been used to prevent and treat many human diseases. Here, we demonstrated that tanshinone IIA prevented ovariectomy-induced bone loss in an in vivo mouse model that closely mimics osteoporosis. In addition, we found that tanshinone IIA inhibited the receptor activator of nuclear factor NF-κB ligand (RANKL)-induced osteoclast differentiation and osteoclastogenesis in vitro. Tanshinone IIA treatment also abrogated RANKL-induced activation of the NF-κB pathway, PI3-kinase/Akt signaling, and the mitogen-activated protein kinase (MAPK) pathways, including nuclear translocation of NF-κB p65 and phosphorylation of IκB, extracellular signal-regulated kinase (ERK), p38, and Akt. Inactivation of these pathways resulted in deceased expression of osteoclastogenesis-related markers. These results suggest that tanshinone IIA, a natural drug, has the potential to treat and prevent bone loss diseases, including postmenopausal osteoporosis.

【 授权许可】

CC BY-NC