The purpose of this study was to explore the potential therapeutic effect of sodium glucuronate (SG) on osteoporosis (OP). To achieve this aim, the optimal concentration of SG for stimulating MC3T3-E1 osteoblast cells derived from the calvaria of neonatal mice was determined using cell counting kit-8 and alkaline phosphatase (ALP) activity assays. Osteogenic markers were analyzed by qRT-PCR and Western blotting. The histopathological morphology of the tibial tissues was performed using hematoxylin and eosin staining. The levels of bone turnover markers (BTMs) were assessed using enzyme-linked immunosorbent assay (ELISA). SG treatment was found to effectively promote osteoblastic differentiation and mineralization in MC3T3-E1 cells, evidenced by enhanced ALP activity, increased calcium deposition, and upregulated expression of key osteogenic markers including runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), and osteopontin (OPN). Moreover, in ovariectomized rats, a model of postmenopausal OP, SG treatment significantly promoted bone formation, regulated the levels of BTMs, and augmented bone mineral density. Consistently, SG upregulated the expression of osteogenic genes (RUNX2, OCN, and OPN) in bone tissue, further supporting its osteogenic potential. Collectively, these findings suggest that SG possesses the ability to stimulate bone formation and may hold promise as a potential agent for the management of OP.
