Objective To investigate the effects of epimedin C combined with bone marrow mesenchymal stem cell transplantation on bone mineral density and bone metabolism in glucocorticoid-induced osteoporosis mice. Methods 75 male C57BL/6 mice were divided into blank control group, model group, epimedin C group, stem cell transplantation group and combination group, with 15 mice in each group. The control group was given intramuscular injection of 0.1mL normal saline, and the other four groups were given intramuscular injection of 0.1mL dexamethasone twice a week for 8 weeks. Bone mineral density, bone structure parameters, serum bone metabolism indexes and AKT protein phosphorylation (p-AKT) were measured. Results Compared with the blank control group, Body weight, bone mineral content (BMC), bone mineral density (BMD), tissue mineral content (TMC), tissue mineral density (TMD), bone volume fraction (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), bone alkaline phosphatase (BALP), N-terminal propeptide of type I procollagen (PINP) and p-AKT of the model group mice decreased significantly, the trabecular separation/spacing (Tb.Sp) in the model group increased significantly, the levels of serum osteocalcin (OCN) and tartaric acid-resistant phosphatase (Trap) in model group were significantly higher (P<0.05). Compared with the model group, the body weight, BMC, BMD, TMC, TMD, BV/TV, Tb.N, Tb.Th of the mice in epimedin C group, stem cell transplantation group and combined group were significantly increased, the phosphorylation levels of BALP, PINP and AKT protein were significantly increased, and the levels of Tb.Sp, serum OCN and Trap were significantly decreased, and the improvement of the above indexes in combined group was better than that in the other two groups (P<0.05). Conclusion Hopidine C combined with bone marrow mesenchymal stem cell transplantation can promote bone formation, increase bone density and improve bone microstructure in glucocorticoid-induced osteoporosis mice, and its mechanism may be related to increasing bone metabolism level and activating PI3K/AKT pathway. |