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Updated: Sep 2, 2025

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
Published on: March 15, 2018
Monascin abrogates RANKL-mediated osteoclastogenesis in RAW264.7 cells via regulating MAPKs signaling pathways
Yin Cheng1, Haixia Liu1, Jing Li2
1Institute of Basic Theory, China Academy of Chinese Medical Sciences, Beijing, China.
Abstract:
Osteoclasts (OCs) are multinucleated cells that play a major role in osteolytic diseases such as osteoporosis. Monascin (Ms) is one of the active substances in the traditional Chinese medicine red yeast rice. Studies have found that red yeast rice can maintain bone health. In this study, the anti-osteoclastogenesis effects of Ms on RANKL-induced RAW264.7 cells were assessed, and the underlying mechanism was investigated. Ms exhibited inhibitory effects on OC differentiation and formation in a dose-dependent manner and suppressed the bone-resorbing activity of mature OCs. Ms blocked OCs-typical genes (c-Fos, NFATc1, CSTK, MMP-9, TRAP, ITG-β3, OSCAR and DC-STAMP). Furthermore, Ms treatment considerably inhibited the activation of MAPKs, JNK and p38. Taken together, Ms suppresses RANKL-induced osteoclastogenesis of RAW264.7 cells by restraining MAPKs signaling pathways and is a potential therapeutic option as a novel OC inhibitor to mitigate bone erosion.
Insights
Monascin (Ms), derived from red yeast rice, effectively inhibits osteoclastogenesis by suppressing key signaling pathways. This finding suggests Ms as a potential therapeutic agent for mitigating bone erosion in diseases like osteoporosis.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Osteoclasts (OCs) are critical in bone resorption and implicated in osteolytic diseases like osteoporosis.
- Red yeast rice, a traditional Chinese medicine, contains Monascin (Ms), known for potential bone health benefits.
Purpose of the Study:
- To investigate the anti-osteoclastogenesis effects of Monascin (Ms) on RANKL-induced RAW264.7 cells.
- To elucidate the underlying molecular mechanisms of Ms's action on osteoclast differentiation and function.
Main Methods:
- RAW264.7 cells were treated with Ms in the presence of RANKL to assess OC differentiation.
- Gene expression analysis was performed for OC-specific markers.
- Mitogen-activated protein kinase (MAPK) signaling pathways (JNK, p38) were analyzed.
Main Results:
- Ms demonstrated dose-dependent inhibition of OC differentiation and formation.
- Ms suppressed the bone-resorbing activity of mature osteoclasts.
- Ms blocked the expression of key osteoclastogenic genes and inhibited MAPK signaling pathways.
Conclusions:
- Monascin (Ms) effectively suppresses RANKL-induced osteoclastogenesis in RAW264.7 cells.
- The mechanism involves the inhibition of MAPK signaling pathways.
- Ms represents a potential therapeutic candidate for treating bone erosion in osteolytic diseases.
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