Conclusion
BADGE treatment ameliorates glucocorticoid-induced osteoporosis by inhibiting PPARγ.
Methods
Thirty-six female C57BL/6J mice were randomly divided into normal (phosphate-buffered saline), model (50 mg/kg dexamethasone sodium phosphate [Dex]), and BADGE (30 mg/kg of BADGE, combined with Dex) groups. All groups received intraperitoneal injections of their treatments, daily for 4 weeks. Protein and mRNA expression levels of gene markers were measured. Micro-computed tomography was used to measure physical parameters of femurs. Bone histomorphology was analyzed by hematoxylin and eosin staining. ELISA was used to measure serum osteocalcin and C-terminal telopeptide of type I collagen (CTX-1).
Results
Glucocorticoid treatment enlarged the marrow fat, concomitant with bone deterioration; BADGE treatment reversed steroid-induced marrow adiposity. Compared with the model group, BADGE treatment improved bone quality and increased bone volume, while increasing osteogenic markers and reducing adipogenic markers at both mRNA and protein levels; moreover, it reduced serum CTX-1 and increased serum osteocalcin.