ETHNOPHARMACOLOGICAL RELEVANCE

Buzhong Yiqi Decoction (BD), a traditional formula in Chinese medicine, is clinically and historically recognized for its effectiveness in reducing physical fatigue and promoting strength, as well as enhancing bone remodeling. Nevertheless, its specific molecular mechanisms related to bone formation have yet to be thoroughly characterized.

AIM OF THE STUDY

This study aims to investigate the effects and mechanisms of BD on osteogenesis in bone marrow mesenchymal stem cells and in a model of tendon-bone junction injury in mice.

MATERIALS AND METHODS

By establishing a mouse model of tendon-bone junction injury, the pathological morphology of the tendon-bone junction in mice was observed. Determining the mechanism of action of BD in regulating osteogenic differentiation through network pharmacology and molecular docking. Flow analysis and osteogenic induction assay were utilized to verify the effect of BD in promoting BMSCs osteogenic differentiation in vitro. In vivo experiments were performed to validate the impact of BD in improving healing after tendon-bone junction injury in mice by promoting osteogenic differentiation.

RESULTS

Bone loss at the heel bone end is an essential pathophysiologic process in the natural healing process after injury to the tendon-bone junction. Using network pharmacology and molecular docking, we identified the PI3K-Akt signaling pathway as a critical mediator of BD-induced osteogenic differentiation. In vitro experiments demonstrated that BD promoted BMSC osteogenesis, while in vivo assays confirmed the enhancement of tendon-bone healing in mice models.

CONCLUSION

These results suggest that BD can effectively promote tendon-bone repair, with the PI3K-Akt pathway playing a crucial role in its therapeutic effects, positioning BD as a promising candidate for improving musculoskeletal injury recovery.