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Dieckol isolated from Eisenia bicyclis extract suppresses RANKL-induced osteoclastogenesis in murine RAW 264.7 cells
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作者 Su-Hyeon Cho Tae-Hyung Kwon +8 位作者 Hoibin Jeong jin sook kim Song-Rae kim Myeong Seon Jeong SeonJu Park Miri Choi Jung-Hee Woo Juhee Ahn Kil-Nam kim 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2022年第6期262-269,共8页
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... 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. 展开更多
关键词 Eisenia bicyclis Dieckol OSTEOCLASTS ERK JNK NF-κB RANKL TRAP Calcitonin receptor NFATc1 RAW 264.7 cell
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