Honokiol Inhibits Osteoclast Differentiation and Function in Vitro
-
- Hasegawa Shin-ichi
- Department of Biological Chemistry, Chubu University
-
- Yonezawa Takayuki
- Research Institute for Biological Functions, Chubu University Department of Nutriproteomics, Graduate School of Medicine, The University of Tokyo
-
- Ahn Jae-Yong
- Department of Biological Chemistry, Chubu University
-
- Cha Byung-Yoon
- Research Institute for Biological Functions, Chubu University
-
- Teruya Toshiaki
- Research Institute for Biological Functions, Chubu University
-
- Takami Masamichi
- Department of Biochemistry, School of Dentistry, Showa University
-
- Yagasaki Kazumi
- Department of Nutriproteomics, Graduate School of Medicine, The University of Tokyo Division of Agriscience and Bioscience, Institute of Symbiotic Science and Technology, Tokyo University of Agriculture and Technology
-
- Nagai Kazuo
- Department of Biological Chemistry, Chubu University Research Institute for Biological Functions, Chubu University
-
- Woo Je-Tae
- Department of Biological Chemistry, Chubu University Research Institute for Biological Functions, Chubu University Department of Nutriproteomics, Graduate School of Medicine, The University of Tokyo
この論文をさがす
抄録
Honokiol, a neolignan, is a physiologically active component of kouboku (Magnolia obovata), a herb used in traditional Chinese medicine. This study investigated the effects of honokiol on the differentiation and function of osteoclasts induced by receptor activator of nuclear factor-κB ligand (RANKL). Honokiol markedly inhibited RANKL-induced tartrate-resistant acid phosphatase (TRAP) activity and the formation of TRAP-positive multinucleated cells in both bone marrow-derived monocytes and RAW264 cells. In experiments to elucidate its mechanism of action, honokiol was found to suppress RANKL-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). The RANKL-induced expressions of c-Fos and nuclear factor of activated T cells-c1 (NFATc1), which are crucial transcriptional factors for osteoclastogenesis, were also reduced by treatment with honokiol. Furthermore, honokiol induced disruption of the actin rings in mature osteoclasts (mOCs) without affecting the cell viability and suppressed osteoclastic pit formation on dentin slices. Taken together, these results suggest that honokiol inhibits osteoclast differentiation by suppressing the activation of MAPKs (p38 MAPK, ERK and JNK), decreasing the expressions of c-Fos and NFATc1, and attenuates bone resorption by disrupting the actin rings in mOCs. Therefore, honokiol could prove useful for the treatment of bone diseases associated with excessive bone resorption.
収録刊行物
-
- Biological & Pharmaceutical Bulletin
-
Biological & Pharmaceutical Bulletin 33 (3), 487-492, 2010
公益社団法人 日本薬学会
- Tweet
キーワード
詳細情報 詳細情報について
-
- CRID
- 1390282679602641024
-
- NII論文ID
- 130000248103
-
- NII書誌ID
- AA10885497
-
- ISSN
- 13475215
- 09186158
-
- NDL書誌ID
- 10582640
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可