Protective effect of LiCl-activated Wnt/β-catenin signaling pathway on glucocorticoid-induced osteoporosis / 第二军医大学学报

ABSTRACT

Objective To investigate the protective effect of lithium chloride (LiCl)-activated Wnt/beta-catenin signaling pathway on glucocorticoid-induced bone loss. Methods C57BL6/J mice were randomly divided into 3 groups. osteoporosis (OP) group and LiCl group were injected intraperitoneally once daily with dexamethasone (50 mg kg). while control group was injected with normal saline. LiCl group was given LiCl (200 mg kg) through water administration. After 5 weeks of treatment, mice were sacrificed within 24 h. Anti-active hela-catenin antibody was used in immuno his to chemical staining to detect the activity of Wnt/beta-cat enin signaling pathway, tone morphology was observed by UK siaining. Meanwhile. bone histomorphometrical parameters were analyzed by microCT. Bone formation and bone resorption of different groups were detected by calcein labeling and TRAP siaining. respectively. Results The protein level of active beta-calenin was higher in LiCl group compared with OP group, tone histomorphometrical parameters including the trabecular bone volume as a percentage of total volume (BV/TV). bone mineral density (HMD), trabecular number (Tb. N) and trabecular space (Tb. Sp) were all significantly improved in LiCl group- even though obvious difference existed lieiween LiCl group and control group (P<0. 05). Calcein labeling showed that new hone formation was markedly improved in LiCl group, but was still lower than that in control group, tone resorption was not significantly changed among three groups as indicated by TRAP siaining. Conclusion LiCl administration effectively activates Wnt/β-catenin signaling pathway in vivo* which improve new bone formation and rescue glucocorticoid-induced bone loss.