Dieckol isolated from Eisenia bicyclis extract suppresses RANKL-induced osteoclastogenesis in murine RAW 264.7 cells

Asian Pacific Journal of Tropical Biomedicine

关键词: eisenia bicyclis;    dieckol;    osteoclasts;    erk;    jnk;    nf-κb;    rankl;    trap;    calcitonin receptor;    nfatc1;    raw 264.7 cell;   

DOI  :  10.4103/2221-1691.345518

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown