Dieckol isolated from Eisenia bicyclis extract suppresses RANKL-induced osteoclastogenesis in murine RAW 264.7 cells
- Author:
Su-Hyeon CHO
1
;
Hoibin JEONG
1
;
Jin KIM
1
;
Song-Rae KIM
1
;
Myeong Seon JEONG
1
;
Seonju PARK
1
;
Miri CHOI
1
;
Kil-Nam KIM
1
;
Su-Hyeon CHO
2
;
Juhee AHN
2
;
Tae-Hyung KWON
3
;
Jung-Hee WOO
4
;
Kil-Nam KIM
5
Author Information
- Publication Type:Journal Article
- Keywords: Calcitonin receptor; Dieckol; Eisenia bicyclis; ERK; JNK; NF-κB; NFATc1; Osteoclasts; RANKL; RAW 264.7 cell; TRAP
- From:Asian Pacific Journal of Tropical Biomedicine 2022;12(6):262-269
- CountryChina
- Language:Chinese
- Abstract: 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.