**5. Conclusions**

To assume the effect of FST on RANKL-mediated osteoclast differentiation, recombinant RANKL protein was used to differentiate murine monocyte/macrophage RAW 264.7 cells as osteoclast precursor cells into osteoclasts. Present results demonstrated that FST inhibited RANKL-induced osteoclastogenesis and reduced the expression of several key osteoclast-regulatory genes through the inactivation of NF-κB. In addition, FST blocked RANKL-induced oxidative stress, which was associated with the activation of Nrf2 signaling pathway. Although the present study provides new insights into the inhibition of osteoclastogenesis by FST, further investigation of the molecular mechanisms underlying this process as well as identification of the bioactive constituents of FST are needed.

**Author Contributions:** Y.H.C., Y.-J.J., C.P. and B.-J.L. conceived and designed the experiments; J.-W.J., H.L., S.H.H. and C.P. performed the experiments; S.Y.J., H.L., G.-Y.K., E.K.P. and J.W.H. analyzed the data; J.-W.J. wrote the paper and Y.H.C. edited the paper.

**Funding:** This research was a part of the project titled 'Development of functional food products with natural materials derived from marine resources (20170285)', funded by the Ministry of Oceans and Fisheries.

**Conflicts of Interest:** The authors declare no conflict of interest.
