Gallic acid from Moutan Cortex promotes osteoblast differentiation and alleviates osteoporosis in mice by targeting HRAS and activating the ERK pathway.

Fracture healing is a complex process where osteoblasts appear as central players in restoring bone integrity through proliferation, differentiation, and mineralization. Previous studies have identified several compounds in cortex moutan, which have been testified to significantly expedite osteoblast proliferation and differentiation. In this study, cell experiments were utilized to screen gallic acid, the key active substance in Moutan Cortex that promote osteogenesis. Subsequently, the targets of gallic acid were analyzed through network pharmacology. As a result, HRAS was a potential target of gallic acid. We further verified the regulation of the RAS/ERK pathway by gallic acid through bioinformatics and Western blot (WB) experiments. Finally, through cell and animal experiments, we demonstrated that Moutan Cortex promoted osteoblast differentiation and relieved osteoporosis.