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Molecules 2018, 23(7), 1598;

Magnolol Inhibits Osteoclast Differentiation via Suppression of RANKL Expression

Herbal Medicine Research Division, Korea Institute of Oriental Medicine, Daejeon 34054, Korea
Author to whom correspondence should be addressed.
Received: 11 June 2018 / Revised: 29 June 2018 / Accepted: 29 June 2018 / Published: 2 July 2018
(This article belongs to the Collection Bioactive Compounds)
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Magnolol, a compound from the traditional Korean herb Magnolia sp., has been exhaustively investigated as a therapeutic agent against several diseases including systemic and local inflammation. We examined the effects of magnolol on osteoclastic differentiation associated with inflammation. Magnolol markedly reduced interleukin (IL)-1-induced osteoclast formation in co-cultures of murine osteoblasts and bone marrow cells, whereas it had no effect on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation in bone marrow macrophage cultures. In osteoblasts, magnolol markedly inhibited both the up-regulation of RANKL expression and the production of prostaglandin E2 (PGE2) in response to IL-1 treatment. Addition of exogenous PGE2 reversed the inhibitory effects of magnolol on IL-1-induced RANKL expression in osteoblasts and osteoclast formation in co-cultures. Magnolol inhibited IL-1-induced PGE2 production, at least in part by suppressing cyclooxygenase-2 (COX-2) expression. Taken together, these results demonstrate that magnolol inhibits IL-1-induced RANKL expression in osteoblasts through suppression of COX-2 expression and PGE2 production, resulting in inhibition of osteoclast differentiation in co-cultures. View Full-Text
Keywords: magnolol; osteoblast; osteoclast; interleukin-1; prostaglandin E2 magnolol; osteoblast; osteoclast; interleukin-1; prostaglandin E2

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Hwang, Y.-H.; Kim, T.; Kim, R.; Ha, H. Magnolol Inhibits Osteoclast Differentiation via Suppression of RANKL Expression. Molecules 2018, 23, 1598.

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