【Objective.】
Steroids are used in clinical practice for a variety of conditions, including immunosuppression. However, steroid-induced osteoporosis due to decreased bone formation (De Nijs., 2008) is a problem (Suzuki et al., 2014). Lactoferrin (LF) is a protein found in breast milk and other sources and has been reported to promote osteoblast differentiation (Icriverzi et al., 2020). In this study, we investigated the therapeutic effect of LF on dexamethasone (DEX)-induced bone loss.
【method】
8-week-old ddy male mice were treated with DEX (2 mg/kg) for 8 weeks. 4 weeks after DEX administration, LF was administered by forced oral administration at a dose of 100 or 300 mg/kg for 6 days per week. 4 weeks after LF administration, femur and tibia were removed and bone strength measurements, CT measurements and mRNA The gene expression levels of bone metabolism markers were examined using RT-PCR.
【Results and Conclusions】
Bone strength after 8 weeks of DEX treatment was significantly lower than that of the untreated group, and LF administration ameliorated the decrease in bone strength. Similarly, CT results showed that LF administration significantly improved the DEX-induced decrease in bone mineral content and bone mineral density. RT-PCR results showed that the gene expression levels of osteogenic markers were significantly decreased by DEX administration and significantly improved by LF administration. These results suggest that LF improves the inhibition of bone loss by DEX through the involvement of the osteogenic system.