| Objective To investigate the effect of polydatin on fracture healing in rats with osteoporotic fracture and its effect on silent information regulator 1 (SIRT1)/forkhead transcription factor O1 (FoxO1) signaling pathway. Methods A rat model of osteoporotic fracture was established, and 48 rats with successful modeling were randomly divided into model group, polydatin low (30 mg/kg), high (60 mg/kg) dose groups, and alendronate sodium (0.5 mg/kg) group. Another 12 rats were taken as control group to construct the fracture model of the same site. After modeling, the rats in each group were given the corresponding drugs by gavage once a day for 8 weeks. Fracturehealing score and bone mineral density (BMD) at fracture site were performed in rats; enzyme linked immunosorbent assay was used to measure the serum levels of C-telopeptide of type I collagen (CTX-Ⅰ), osteocalcin (OC), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β); HE staining was used to observe the pathological changes of bone tissue; the mRNA levels of SIRT1 and FoxO1 in bone tissue were detected by fluorescence quantitative PCR; Western blot was used to detect the protein levels of SIRT1 and FoxO1 in bone tissue. Results Compared with model group, the pathological changes of bone tissue in thepolydatin low and high dose groups were gradually alleviated, the fracture healing score, BMD at the fracture site, the levels of OCin serum, and mRNA and protein levels of SIRT1 and FoxO1 in bone tissue were increased successively, CTX-Ⅰ, TNF-α, IL-1β levels was decreased successively (P<0.05); there were no significant differences in bone pathological changes and various indexes between alendronate sodium group and polydatin high dose group (P>0.05). Conclusion Polydatin can reduce inflammatory response, improve BMD and promote fracture healing in rats with osteoporotic fracture, and its mechanism may be related to the activation of SIRT1/FoxO1 signaling pathway. |