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来源于威灵仙的三萜皂苷W3通过抑制MAPKs和NF-κB信号通路的激活来抑制破骨细胞分化。

Triterpenoid Saponin W3 from Anemone flaccida Suppresses Osteoclast Differentiation through Inhibiting Activation of MAPKs and NF-κB Pathways.

作者信息

Kong Xiangying, Yang Yue, Wu Wenbin, Wan Hongye, Li Xiaomin, Zhong Michun, Su Xiaohui, Jia Shiwei, Lin Na

机构信息

1. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, 100700 Beijing, China.

2. Guangzhou Kanghe Pharmaceutical Limited Company, 511440 Guangzhou, China.

出版信息

Int J Biol Sci. 2015 Aug 15;11(10):1204-14. doi: 10.7150/ijbs.12296. eCollection 2015.

DOI:10.7150/ijbs.12296
PMID:26327814
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4551756/
Abstract

Excessive bone resorption by osteoclasts within inflamed joints is the most specific hallmark of rheumatoid arthritis. A. flaccida has long been used for the treatment of arthritis in folk medicine of China; however, the active ingredients responsible for the anti-arthritis effects of A. flaccida are still elusive. In this study, W3, a saponin isolated from the extract of A. flaccida was identified as the major active ingredient by using an osteoclast formation model induced by receptor activator of nuclear factor kappa-B ligand (RANKL). W3 dose-dependently suppressed the actin ring formation and lacunar resorption. Mechanistic investigation revealed that W3 inhibited the RANKL-induced TRAF6 expression, decreased phosphorylation of mitogen-activated protein kinases (MAPKs) and IκB-α, and suppressed NF-κB p65 DNA binding activity. Furthermore, W3 almost abrogated the expression of c-Fos and nuclear factor of activated T cells (NFATc1). Therefore, our results suggest that W3 is a potential agent for treating lytic bone diseases although further evaluation in vivo and in clinical trials is needed.

摘要

炎症关节内破骨细胞过度的骨吸收是类风湿性关节炎最具特异性的标志。在中国民间医学中，威灵仙长期以来一直用于治疗关节炎；然而，威灵仙抗关节炎作用的活性成分仍不明确。在本研究中，通过使用核因子κB受体激活剂配体（RANKL）诱导的破骨细胞形成模型，从威灵仙提取物中分离出的皂苷W3被确定为主要活性成分。W3呈剂量依赖性地抑制肌动蛋白环形成和陷窝吸收。机制研究表明，W3抑制RANKL诱导的TRAF6表达，降低丝裂原活化蛋白激酶（MAPKs）和IκB-α的磷酸化，并抑制NF-κB p65 DNA结合活性。此外，W3几乎消除了c-Fos和活化T细胞核因子（NFATc1）的表达。因此，我们的结果表明，W3是一种治疗溶骨性骨疾病的潜在药物，尽管需要在体内和临床试验中进行进一步评估。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e36/4551756/e854ffcae7f7/ijbsv11p1204g010.jpg
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