| Objective To investigate the effect of autologous platelet-rich plasma (PRP) on fracture healing in osteoporosis (OP) rats. Methods Sixty SD rats were taken and randomly divided into normal fracture group, model group, PRP group, DAPT group (Notch pathway inhibitor DAPT), PRP+DAPT group, with twelve rats in each group. The normal fracture group was treated with intramedullary fixation of the right femoral shaft fracture to establish a fracture model, while the other groups of rats were treated with retinoic acid (70 mg/kg) gavage and intramedullary fixation of the right femoral shaft fracture to establish an OP fracture model. The PRP group prepared an autologous PRP gel solution and injected it between the fracture ends. The DAPT group was injected with the Notch pathway inhibitor DAPT via the tail vein, and the PRP+DAPT group was given DAPT through tail vein while giving PRP. After 6 weeks of administration in each group, the fracture healing was observed by X-ray; Micro-CT method was used to detect changes in callus bone density, callus volume/total volume, number of bone trabeculae and trabecular bone thickness; ELISA method was used to detect the levels of serum osteocalcin (OCN), bone alkaline phosphatase (BAP), platelet-derived growth factor (PDGF), transforming growth factor-β (TGF-β) and insulin-like growth factor 1 receptor (IGF-1R); calcium-cobalt alkaline phosphatase staining and TRAP staining method were used to detect the numbers of osteoblasts and osteoclasts; immunohistochemical method was used to detect the positive expression level of Notch1 in the callus tissue; Western blot was used to detect the protein expression of bone morphogenetic protein (BMP), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) in the callus tissue. Results Compared with rats in the normal fracture group, OP fracture model rats had less callus formation, delayed fracture healing, decreased serum osteogenic active cytokine secretion, bone volume, the density of the callus, the number and thickness of the bone trabecula were all reduced, the number of osteoblasts was less, the number of osteoclasts formed more, Notch1 and its BMP and OPG mediated bone formation proteins were inhibited, the activity of osteoclast formation-related protein RANKL increased (P<0.05). Compared with the model group, the PRP group could promote callus formation and bone healing, promote the expression of osteogenesis-related factors, activate Notch1, and activate the bone formation pathway mediated by it and weaken the osteoclast formation pathway (P<0.05). DAPT could block the above-mentioned effects of PRP. Conclusion The role of autologous PRP in promoting bone mass increase and fracture healing in OP induced fracture rats may be related to promoting the activation of the Notch1 pathway. |