A Study on the Protective Effect and Mechanism of Polygonatum sibiricum Aqueous Extract on Osteoporosis in Rats

Introduction: Glucocorticoid-induced osteoporosis (GIOP) is the most common cause of drug-induced osteoporosis. The impact of PSAE on the GIOP remains uncertain. Consequently, this study aimed to examine the protective effects of PSAE against osteoporosis induced by dexamethasone in glucocorticoid-treated rats. Methods: A total of 50 3-month-old female SD rats were randomly divided into blank, model, low-dose PSAE, high-dose PSAE, and PSAE control groups. Serum phosphorus, calcium, Alkaline Phosphatase (ALP), and Tartrate-Resistant Acid Phosphatase 5b (TRACP-5b) activities were measured by a detection kit, respectively. The femoral bone density, microstructure, tissue pathology, and biomechanical properties changes were measured by Dual-energy X-ray Absorptiometry, Micro-computed tomography, HE staining, and Bone Compression Mechanics Experiment, respectively. Finally, the expression of OPG, RANKL, and RANK mRNA and protein in bone tissue was detected by qPCR and WB. Results: Compared with the model group, PSAE significantly increased the BMD value (20.5% in LPSAE and 12.1% in HPSAE), increased the maximal stress and maximal loading values of the bone tissues (44.3% in LPSAE), significantly decreased the expression of RANKL gene and protein (52.6%, 54.5% in LPSAE), differentially decreased the expression of RANK gene and protein, and simultaneously increased the expression of OPG protein. Discussion: The results indicate that PSAE improved osteoporosis pathology and bone microarchitecture, and suggest that it functions through the OPG/RANKL/RANK signaling pathway. Conclusion: PSAE ameliorated dexamethasone-induced osteoporosis in rats, which may be related to the involvement of PSAE in regulating the homeostasis of bone metabolism and further inhibiting the role of osteoclast differentiation mediated by the OPG/RANKL/RANK signaling pathway.