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Furosin, an ellagitannin, suppresses RANKL-induced osteoclast differentiation and function through inhibition of MAP kinase activation and actin ring formation
Authors:Park Eui Kyun  Kim Myung Sunny  Lee Seung Ho  Kim Kyung Hee  Park Ju-Young  Kim Tae-Ho  Lee In-Seon  Woo Je-Tae  Jung Jae-Chang  Shin Hong-In  Choi Je-Yong  Kim Shin-Yoon
Institution:Skeletal Diseases Genomic Research Center, Kyungpook National University Hospital, Kyungpook National University, Daegu 700-412, Republic of Korea.
Abstract:Phenolic compounds including tannins and flavonoids have been implicated in suppression of osteoclast differentiation/function and prevention of bone diseases. However, the effects of hydrolysable tannins on bone metabolism remain to be elucidated. In this study, we found that furosin, a hydrolysable tannin, markedly decreased the differentiation of both murine bone marrow mononuclear cells and Raw264.7 cells into osteoclasts, as revealed by the reduced number of tartrate resistant acid phosphatase (TRAP)-positive multinucleated cells and decreased TRAP activity. Furosin appears to target at the early stage of osteoclastic differentiation while having no cytotoxic effect on osteoclast precursors. Analysis of the inhibitory mechanisms of furosin revealed that it inhibited the receptor activator of nuclear factor-kappaB ligand (RANKL)-induced activation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK)/activating protein-1 (AP-1). Furthermore, furosin reduced resorption pit formation in osteoclasts, which was accompanied by disruption of the actin rings. Taken together, these results demonstrate that naturally occurring furosin has an inhibitory activity on both osteoclast differentiation and function through mechanisms involving inhibition of the RANKL-induced p38MAPK and JNK/AP-1 activation as well as actin ring formation.
Keywords:Furosin  Osteoclastogenesis  p38MAPK  JNK  AP-1  Actin ring
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