Icariin attenuates glucocorticoid-induced bone deteriorations, hypocalcemia and hypercalciuria in mice.

OBJECTIVE This study was performed to investigate bone deteriorations and calcium homeostasis of GIOP mice in response to the treatment of icariin. METHODS The biomarkers in serum and urine were measured, tibias were taken for the measurement on bone calcium, gene expression, histomorphology and micro-CT. RESULTS Glucocorticoid-treated facilitated to induce hypocalcemia and hypercalciuria in mice, and icariin-treated showed a greater increase in serum calcium and decrease in urine calcium. Icariin reversed DXM-induced trabecular deleterious effects and stimulated bone remodeling, including an increase in bone calcium, OCN and FGF-23 and a decrease in a critical bone resorption markers CTX and TRAP-5b. H&E staining and micro-CT showed the increased disconnections and separation among growth plate and trabecular bone network as well as the reduction of trabecular bone mass of primary and secondary spongiosa throughout the proximal metaphysis of tibia in DXM group. Importantly, icariin reversed DXM-induced trabecular deleterious effects and stimulated bone remodeling. Moreover, the results showed that the mRNA expression of MMP-9 and CAII was significantly increased in DXM group compared with control group. Icariin treatment could suppress the expression of MMP-9 and CAII in the tibia of mice. CONCLUSIONS The present study demonstrated the protective effects of icariin against bone deteriorations, hypocalcemia and hypercalciuria in experimentally DIOP mice. Furthermore, these results provided further evidence to support the dual role of icariin as a bone formation enhancer and bone resorption inhibitor.