4.6 Article

Achyranthes bidentata polysaccharide suppresses osteoclastogenesis and bone resorption via inhibiting RANKL signaling

Journal

JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 119, Issue 6, Pages 4826-4835

Publisher

WILEY
DOI: 10.1002/jcb.26682

Keywords

Achyranthes bidentata polysaccharide; bone resorption; MAPK; osteoclast

Funding

  1. National Key Technology Research and Development Program of China [2017YFC1103300]
  2. Nature Science Foundation of China [81572164]
  3. Qingdao municipal health and Family Planning Commission [2016-WJZD130]
  4. University Science and Technology Research Project of Guangxi Province [KY2015YB054]
  5. Natural Science Foundation of Guangxi Province [2016GXNSFAA380295]
  6. Guangxi Scientific Research and Technology Development Plan Project [GKG13349003, 1598013-15]
  7. Australian Health and Medical Research Council [110782, 1027932]
  8. Western Australia Medical & Health Research Infrastructure Fund
  9. Arthritis Australia Foundation
  10. University of Western Australia (UWA) Research Collaboration Awards

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Osteoclasts are highly differentiated multinucleated giant cells that play fundamental roles in bone resorption and in the pathogenesis of osteolytic conditions, such as osteoporosis and cancer-induced bone loss. Achyranthes bidentata polysaccharide (ABP) is a hydrophilic compound with anti-oxidation and anti-aging characteristics. The impact of ABP on RANKL-induced osteoclast formation and bone resorption has not been assessed, hence, in this study we investigated the effect of ABP on osteoclast formation and resorption in murine bone marrow derived osteoclasts. We found that ABP was able to suppress RANKL-induced osteoclast differentiation and bone resorption activity at concentrations above 6.5 mu M, while demonstrating no cytotoxicity at concentrations up to 10 mu M. The actions of ABP were mediated through inhibition of RANKL-induced c-Fos and NFATc1 gene and protein expression. Furthermore, we found that ABP suppressed NFATc1 transcriptional activity, and the phosphorylation of MAPK pathways induced by RANKL. Collectively, ABP attenuates RANKL-mediated osteoclast activity and signaling, and might serve as a potential therapeutic candidate for preventing bone loss related diseases.

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