4.4 Article

Isobavachalcone inhibits RANKL-induced osteoclastogenesis via miR-193-3p/NF-κB/NFATc1 signaling pathway in BMMs cells

Journal

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
Volume 87, Issue 9, Pages 960-971

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/bbb/zbad075

Keywords

isobavachalcone; osteoclast; RANKL; NF-kappa B; miR-193-3p

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In this study, it was discovered that isobavachalcone, derived from the traditional Chinese herb Psoralea corylifolia Linn, can inhibit osteoclastogenesis and bone resorption. The mechanism involves the suppression of NF-κB activation and downregulation of osteoclastic-specific genes and proteins. This suggests that isobavachalcone may have potential as a therapeutic compound for the treatment of osteoporosis and other metabolic bone diseases.
Inhibition of extensive osteoclastogenesis and bone resorption is considered a potential therapeutic target for the treatment of osteoporosis. Isobavachalcone (IBC) is derived from the traditional Chinese herb Psoralea corylifolia Linn. We showed that IBC dose-dependently suppressed receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastogenesis in bone marrow monocyte/macrophage (BMMs) and osteoclastic bone-resorption function without cytotoxicity at a dose of no more than 8 & mu;min vitro. Mechanistically, the results of western blot and quantitative real-time polymerase chain reaction (qRT-PCR) indicated that IBC inhibited the RANKL-induced degradation of I & kappa;B & alpha; and phosphorylation of nuclear factor kappa B (NF-& kappa;B) in BMMs, and subsequently downregulated the expression of osteoclastic-specific genes and osteoclastogenesis-related proteins. TRAP staining and qRT-PCR showed that IBC can inhibit osteoclast differentiation by down-regulating the expression of miR-193-3p on osteoclast differentiation. Overall, our findings suggest that IBC may serve as a promising compound for the treatment of osteoporosis and other metabolic bone diseases.

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