Maackiain dampens osteoclastogenesis via attenuating RANKL-stimulated NF-κB signalling pathway and NFATc1 activity

  • J Cell Mol Med. 2020 Nov;24(21):12308-12317. doi: 10.1111/jcmm.15647.
Yuhao Liu  1  2  3 ,  Weizai Zeng  4 ,  Chao Ma  3 ,  Ziyi Wang  2 ,  Chao Wang  2 ,  Shaobin Li  3 ,  Wei He  1  3 ,  Qingwen Zhang  1  3 ,  Jiake Xu  1  2 ,  Chi Zhou  1  3
Affiliations
  • 1. The First Affiliated Hospital, Institute of Orthopedics, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 2. School of Biomedical Sciences, University of Western Australia, Perth, Australia.
  • 3. The First Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 4. Chinese Medicine Hospital of Zengcheng District, Guangzhou, China.
PMID: 32939977 DOI: 10.1111/jcmm.15647
Abstract

Osteolytic diseases are typified by over-enhanced formation and resorbing function of osteoclasts and have a major impact on human health. Inhibition of osteoclastic differentiation and function is a key strategy for clinical therapy of osteolytic conditions. Maackiain is a natural compound extracted from Sophora flavescens, which has been applied to anti-allergic and anti-tumour treatments. The present results showed that Maackiain could restrain receptor activator of nuclear factor-κB ligand (RANKL)-stimulated osteoclast formation and hydroxyapatite resorption dose-dependently, and interrupt the structures of F-actin belts in the mature osteoclasts. It also repressed the expressions of osteoclast-specific genes and proteins. Furthermore, Maackiain could inhibit RANKL-stimulated NF-κB and calcium signalling pathways, and dampen Nuclear factor of activated T cell cytoplasmic 1 activity, protein expression and translocation into the nucleus. These results revealed that Maackiain may have a potential therapeutic effect on osteoclast-related disorders.

Keywords
maackiain; nuclear factor of activated T cells 1; nuclear factor-κB; osteoclast; receptor activator of nuclear factor-κB ligand.
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