Repair of Osteoporotic Bone Defects in Rats Via the Sirtuin 1-Wnt/β-catenin Signaling Pathway by Novel Icariin/Porous Magnesium Alloy Scaffolds

The slow rate of bone regeneration and repair in osteoporotic defects is one of the difficulties of clinical work. To prepare a novel icariin (ICA)/porous magnesium alloy scaffold and to investigate its effectiveness and possible mechanism in repairing osteoporotic bone defects, bilateral ovariectomy was performed on Sprague-Dawley rats. Then, a cylindrical bone defect was created in the model, and a novel ICA/porous magnesium alloy scaffold was prepared and implanted into the defect. Eight or 12 weeks after repairing, specimens and micro-computed tomography (CT) data were collected. Microscopic observation was fulfilled through hematoxylin and eosin, Goldner, Masson, periodic acid-Schiff, and Sirius red staining. The expression of proteins was detected by immunohistochemical staining. The novel ICA/porous magnesium alloy scaffold was noncytotoxic and biologically safe. After it was implanted into the defect for 8 or 12 weeks, the surface color and smoothness, depth, and area of the defect were better than those in the control group. Besides, there was sufficient osteoid tissue, more mineralized bones, more collagen fibers, and more polysaccharide components in the defect repaired with the ICA/porous magnesium alloy scaffold. These conditions are closer to those of real bones. Moreover, the repair effect improved with the repair time. Compared with those in the control group, the expression levels of Sirtuin 1(SIRT1), Wnt5a, β-catenin, glycogen synthase kinase 3β, alkaline phosphatase, runt-related transcription factor 2, bone morphogenetic protein-2, and osteocalcin proteins were elevated in bone tissue after the scaffold was implanted into the defect for 8 weeks (all < 0.05). The novel ICA/porous magnesium alloy scaffold promotes the repair of osteoporotic bone defects in rats, a process that may be achieved through activation of the SIRT1-Wnt/β-catenin signaling pathway.