Related Experiment Video
Updated: Nov 7, 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
Galangin suppresses RANKL-induced osteoclastogenesis via inhibiting MAPK and NF-κB signalling pathways
Xiucheng Li1, Jiawei Jiang1, Zhifan Yang1
1Department of Orthopaedics, Shaoxing People's Hospital, Zhejiang University School of Medicine, Shaoxing, China.
Abstract:
Osteoclasts play a critical role in osteoporosis; thus, inhibiting osteoclastogenesis is a therapeutic strategy for osteoporosis. Galangin, a natural bioflavonoid extracted from a traditional Chinese herb, possesses a variety of biological activities, including anti-inflammation and anti-oxidation. However, its effects on osteoporosis have not been elucidated. In this study, we found that galangin treatment dose-dependently decreased osteoclastogenesis in bone marrow-derived macrophages (BMMs). Moreover, during osteoclastogenesis, osteoclast-specific genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (CtsK), ATPase, H + transporting, lysosomal V0 subunit D2 (V-ATPase d2) and dendritic cell-specific transmembrane protein (DC-STAMP), were down-regulated by galangin treatment. Furthermore, the results of the pit formation assay and F-actin ring staining revealed impaired osteoclastic bone resorption in the galangin-treated group compared with that in the control group. Additionally, galangin treatment also inhibited the phosphorylation of p38 and ERK of MAPK signalling pathway, as well as downstream factors of NFATc1, C-Jun and C-Fos. Consistent with our in vitro results, galangin suppressed lipopolysaccharide (LPS)-induced bone resorption via inhibition of osteoclastogenesis. Taken together, our findings provide evidence that galangin is a promising natural compound for the treatment of osteoporosis and may be associated with the inhibition of MAPK and NF-κB signalling pathways.
Insights
Galangin, a natural compound, effectively inhibits osteoclast formation and bone resorption, offering a potential new treatment for osteoporosis by targeting key signaling pathways.
Area of Science:
- Biochemistry
- Pharmacology
- Cell Biology
Background:
- Osteoclasts are crucial in osteoporosis pathogenesis.
- Inhibiting osteoclastogenesis is a therapeutic target for osteoporosis.
- Galangin, a natural bioflavonoid, has anti-inflammatory and anti-oxidative properties, but its effect on osteoporosis is unknown.
Purpose of the Study:
- To investigate the effects of galangin on osteoclastogenesis and bone resorption.
- To elucidate the molecular mechanisms underlying galangin's action in osteoporosis.
Main Methods:
- Bone marrow-derived macrophages (BMMs) were treated with galangin to assess osteoclastogenesis.
- Osteoclast-specific gene expression (TRAP, CtsK, V-ATPase d2, DC-STAMP) was analyzed.
- Pit formation assays and F-actin ring staining evaluated osteoclastic bone resorption.
- MAPK signaling pathway (p38, ERK) and downstream factors (NFATc1, C-Jun, C-Fos) were assessed.
- Lipopolysaccharide (LPS)-induced bone resorption in vivo was examined.
Main Results:
- Galangin dose-dependently decreased osteoclastogenesis in BMMs.
- Galangin down-regulated key osteoclast-specific genes.
- Impaired osteoclastic bone resorption was observed in galangin-treated groups.
- Galangin inhibited MAPK signaling pathway phosphorylation and downstream factors.
- Galangin suppressed LPS-induced bone resorption by inhibiting osteoclastogenesis.
Conclusions:
- Galangin effectively inhibits osteoclastogenesis and bone resorption.
- Galangin's mechanism involves the inhibition of MAPK and NF-κB signaling pathways.
- Galangin shows promise as a natural therapeutic compound for osteoporosis treatment.
Related Concept Videos
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
The JAK-STAT Signaling Pathway
TGF - β Signaling Pathway
MAPK Signaling Cascades
Co-activators and Co-repressors
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...

