| Objective To explore the effect of diosmetin on the healing of osteoporotic bone defects by regulating Hedgehog signaling pathway. Methods SD rats were divided into sham operation group, model group, low-dose group (50 mg/kg diosmetin), high-dose group (100 mg/kg diosmetin), and high-dose+cyclopamine group (10mg/kg cyclopamine, a Hedgehog signaling pathway specific inhibitor), with 10 rats in each group. Rat model of osteoporosis (OP) was built by removal of bilateral ovaries of the rat, and the bone defect model was built on this basis. After modeling, the corresponding drugs were given by gavage. Dual-energy X-ray absorptiometry was used to detect bone mineral density (BMD) in the callus of rats. HE staining was used to observe the pathology of the bone defect area in rats. Tartrate-resistant acid phosphatase (TRAP) staining was used to observe the osteoclasts in the bone defect area of rats. qRT-PCR was used to detect the expression of osteoblast-specific transcription factor (Osterix) and Runt-related transcription factor 2 (RUNX2) in rat bone defect area. The expression levels of Sonic hedgehog (Shh), Gli family zinc finger-1 (GLI1), Ptched 1 (Ptch1), Osterix, and RUNX2 in the tissues of bone defect area were determined with Western blotting detection. Results Compared to those in the sham operation group, BMD at the callus, the number of trabeculae, the expressions of Osterix, Runx2, SHH, GLI1, and Ptch1 were significantly lower in the model group, while the number of TRAP positive cells was significantly higher (P<0.05). Compared to those in the model group, BMD at the callus, the number of trabeculae, the expressions of Osterix, Runx2, SHH, GLI1, and Ptch1 were significantly higher in the low-dose group and high-dose group, while the number of TRAP positive cells was significantly lower (P<0.05). Cyclopamine reversed the effect of diosmetin on the healing of osteoporotic bone defects. Conclusion Diosmetin promotes the healing of osteoporotic bone defects by activating the Hedgehog pathway. |