LAUSR

Osteoporotic fracture healing is a complex clinical issue. The present study was conducted to investigate the repair properties of 11R-VIVIT on osteoporotic fractures and to examine the potential effects of 11R-VIVIT on osteoporotic bone marrow-derived mesenchymal stem cells (BMSCs), A rat model of osteoporotic femoral fracture was established, and the effects of the daily local injection of 11R-VIVIT or saline on fracture repairing were evaluated by micro-CT scans and H&E staining. Moreover, BMSCs from osteoporotic rats were treated with 11R-VIVIT, and the osteogenic and adipogenic differentiation of BMSCs was evaluated. The results revealed that 11R-VIVIT promoted bone formation and increased fracture healing. In addition, 11R-VIVIT promoted the differentiation of osteoporotic BMSCs into osteoblasts rather than adipocytes. Furthermore, mechanistic analysis revealed that 11R-VIVIT promoted autophagy by blocking the protein kinase B (AKT)/nuclear factor of activated T-cells (NFATc1) signaling pathway. Consistently, the activation and inhibition of autophagy using rapamycin and LY294002 confirmed the regulatory effects of 11R-VIVIT on autophagy. On the whole, the findings of the present study demonstrate that 11R-VIVIT promotes fracture healing in osteoporotic rats and enhances the osteogenic differentiation of osteoporotic BMSCs by dysregulating the AKT/NFATc1 signaling pathway.