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Original Research

Sarsasapogenin Suppresses RANKL-Induced Osteoclastogenesis in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo

ORCID Icon, , , , , , , , , , & show all
Pages 3435-3447 | Published online: 24 Aug 2020
 

Abstract

Introduction

Osteoclasts are giant polynuclear cells; their main function is bone resorption. An increased number of osteoclasts and enhanced bone resorption exert significant effects on osteoclast-related bone-lytic diseases, including osteoporosis. Given the limitations of current therapies for osteolytic diseases, it is urgently required to develop safer and more effective alternatives. Sarsasapogenin, a major sapogenin from Anemarrhena asphodeloides Bunge, possesses potent antitumor effects and inhibits NF-κB and MAPK signaling. However, the manner in which it affects osteoclasts is unclear.

Methods

We investigated the effects of anti-osteoclastogenic and anti-resorptive of sarsasapogenin on bone marrow-derived osteoclasts.

Results

Sarsasapogenin inhibited multiple RANKL-induced signaling cascades, thereby inhibiting the induction of key osteoclast transcription factor NFATc1. The in vivo and in vitro results were consistent: sarsasapogenin treatment protected against bone loss in a mouse osteolysis model induced by lipopolysaccharide.

Conclusion

Our research confirms that sarsasapogenin can be used as a new treatment for osteoclast-related osteolytic diseases.

Acknowledgments

This study was supported by the National Science Foundation of China (Grant No. 81871801), Zhejiang Basic Public Welfare Research Project (LGF18H060010), Natural Science Foundation of Zhejiang Province (Grant No. LQ19H060001), Projects of Medical and Health Technology Development Program in Zhejiang Province (2018KY824), and Zhejiang Medical and Health Science and Technology Project (2019KY712).

Disclosure

Jiaxuan Peng, Kangxian Zhao and Jiling Zhu should be regarded as co-first authors.

The authors have no conflicts of interest.