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Dieckol isolated from Eisenia bicyclis extract suppresses RANKL-induced osteoclastogenesis in murine RAW 264.7 cells
Su-Hyeon Cho1, Tae-Hyung Kwon2, Hoibin Jeong3, Jin Sook Kim3, Song-Rae Kim3, Myeong Seon Jeong3, SeonJu Park3, Miri Choi3, Jung-Hee Woo4, Juhee Ahn5, Kil-Nam Kim6
1 Chuncheon Center, Korea Basic Science Institute; Department of Medical Biomaterials Engineering, College of Biomedical Sciences, Kangwon National University, Chuncheon 24341, Republic of Korea
2 Department of Research and Development, Chuncheon Bio-industry Foundation, Chuncheon, Republic of Korea
3 Chuncheon Center, Korea Basic Science Institute, Chuncheon 24341, Republic of Korea
4 Marine Industry Research Institute for East se rim, Uljin-gun, Gyeongsangbuk-do, Republic of Korea
5 Department of Medical Biomaterials Engineering, College of Biomedical Sciences, Kangwon National University, Chuncheon 24341, Republic of Korea
6 Chuncheon Center, Korea Basic Science Institute, Chuncheon 24341; Department of Bio-analysis Science, University of Science & Technology, Daejeon, 34113, Republic of Korea
Correspondence Address:
Juhee Ahn
Department of Medical Biomaterials Engineering, College of Biomedical Sciences, Kangwon National University, Chuncheon 24341
Republic of Korea
Kil-Nam Kim
Chuncheon Center, Korea Basic Science Institute, Chuncheon 24341; Department of Bio-analysis Science, University of Science & Technology, Daejeon, 34113
Republic of Korea
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/2221-1691.345518
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Objective: To demonstrate the effect of dieckol from Eisenia bicyclis on osteoclastogenesis using RAW 264.7 cells. Methods: Murine macrophage RAW 264.7 cells were subjected to dieckol treatment, followed by treatment with receptor activator of nuclear factor kappa-B ligand (RANKL) to induce osteoclastogenesis. Tartrate-resistant acid phosphatase (TRAP) activity was examined using a TRAP activity kit. Western blotting analysis was conducted to examine the level of osteoclast- related factors, including TRAP and calcitonin receptor (CTR), transcriptional factors, including c-Fos, c-Jun, and nuclear factor of activated T cells cytoplasmic 1 (NFATc1), nuclear factor kappa-B (NF-κB), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). Immunofluorescence staining was conducted to examine the expression of c-Fos, c-Jun, and NFATc1. Results: Among the four phlorotannin compounds present in Eisenia bicyclis, dieckol significantly hindered osteoclast differentiation and expression of RANKL-induced TRAP and CTR. In addition, dieckol downregulated the expression levels of c-Fos, c-Jun, NFATc1, ERK, and JNK, and suppressed NF-κB signaling. Conclusions: Dieckol can suppress RANKL-induced osteoclastogenesis. Therefore, it has therapeutic potential in treating osteoclastogenesis- associated diseases. |
