Abstract

Background: Osteoporosis is a common skeletal disorder characterized by increased bone fragility and fracture risk. Current treatments are limited, necessitating the development of novel therapeutic agents.

Methods: RAW264.7 cells were treated with CBT (0, 10, 20, 40 μg/mL) and stimulated with RANKL to induce osteoclast differentiation. Cell viability was assessed by CCK-8 assay, while osteoclast differentiation was evaluated through TRAP staining. Immunoblot analysis was conducted to confirm the underlying mechanism.

Results: Columbianetin significantly inhibited the differentiation and activity of osteoclasts. Furthermore, Columbianetin was found to suppress autophagy in osteoclasts. Mechanically, Columbianetin exerted its effects by inhibiting the SGK1/FOXO3a signaling pathway.

Conclusion: Columbianetin effectively inhibits osteoclast differentiation and autophagy by modulating the SGK1/FOXO3a pathway, highlighting its potential as a therapeutic agent for osteoporosis treatment.