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Honokiol inhibits osteoclast differentiation and function in vitro.
Biol Pharm Bull. 2010; 33(3):487-92.BP

Abstract

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-kappaB 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.

Authors+Show Affiliations

Department of Biological Chemistry, Chubu University, Kasugai, Aichi 487-8501, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20190414

Citation

Hasegawa, Shin-Ichi, et al. "Honokiol Inhibits Osteoclast Differentiation and Function in Vitro." Biological & Pharmaceutical Bulletin, vol. 33, no. 3, 2010, pp. 487-92.
Hasegawa S, Yonezawa T, Ahn JY, et al. Honokiol inhibits osteoclast differentiation and function in vitro. Biol Pharm Bull. 2010;33(3):487-92.
Hasegawa, S., Yonezawa, T., Ahn, J. Y., Cha, B. Y., Teruya, T., Takami, M., Yagasaki, K., Nagai, K., & Woo, J. T. (2010). Honokiol inhibits osteoclast differentiation and function in vitro. Biological & Pharmaceutical Bulletin, 33(3), 487-92.
Hasegawa S, et al. Honokiol Inhibits Osteoclast Differentiation and Function in Vitro. Biol Pharm Bull. 2010;33(3):487-92. PubMed PMID: 20190414.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Honokiol inhibits osteoclast differentiation and function in vitro. AU - Hasegawa,Shin-Ichi, AU - Yonezawa,Takayuki, AU - Ahn,Jae-Yong, AU - Cha,Byung-Yoon, AU - Teruya,Toshiaki, AU - Takami,Masamichi, AU - Yagasaki,Kazumi, AU - Nagai,Kazuo, AU - Woo,Je-Tae, PY - 2010/3/2/entrez PY - 2010/3/2/pubmed PY - 2010/9/21/medline SP - 487 EP - 92 JF - Biological & pharmaceutical bulletin JO - Biol Pharm Bull VL - 33 IS - 3 N2 - 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-kappaB 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. SN - 1347-5215 UR - https://www.unboundmedicine.com/medline/citation/20190414/Honokiol_inhibits_osteoclast_differentiation_and_function_in_vitro_ L2 - http://joi.jlc.jst.go.jp/JST.JSTAGE/bpb/33.487?from=PubMed DB - PRIME DP - Unbound Medicine ER -