期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 25, 期 1, 页码 49-54出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2015.01.010
关键词
Saikosaponin a; Osteoclast; RANKL; NF-kappa B; MAPK
资金
- Natural Science Foundation of China [81373665]
- Industrial Technology Research and Development Fund of Guangdong Province [2013B021800226]
Inflammatory cytokines play an important role in osteoclastogenesis. Saikosaponin a (SSa) possesses anti-inflammatory activity. However, the role of SSa in osteoporosis is still unclear. Therefore, the objective of this study was to investigate the effects of SSa on receptor activator of the nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis and signaling pathway by in vitro assay. In mouse bone marrow monocytes (BMMs), SSa suppressed RANKL plus macrophage colony-stimulating factor (M-CSF)-induced osteodast differentiation in a dose-dependent manner. Moreover, SSa decreased osteoclastogenesis-related marker proteins expression, including NFATcl, c-fos and cathepsin K At molecular levels, SSa inhibited RANKL-induced I kappa B alpha phosphotylation, p65 phosphorylation and NF-kappa B luciferase activity in RAW264.7 cells. And SSa also suppressed RANKL-induced p-38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) phosphorylation. Taken together, these findings suggest that SSa suppresses osteoclastogenesis through inhibiting RANKL-induced p-38, ERK, JNK and NF-kappa B activation. SSa is a novel agent in the treatment of osteodast-related diseases, such as osteoporosis. (C) 2015 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据