Effects of lactoferrin on dexamethasone-induced osteoporosis in mice

Abstract

Glucocorticoids (GCs) have strong anti-inflammatory properties and are widely used to treat many inflammatory and autoimmune diseases. However, long-term GC therapy is limited by the associated serious side effects, such as osteoporosis. In the present study, we investigated the preventive effects of lactoferrin (LF) on dexamethasone (DEX)-induced bone loss in mice. Male ICR mice were treated with vehicle, DEX, or DEX and LF for 4 weeks. The femurs of all mice were analyzed using microcomputed tomography (μCT). A number of indices, including bone mineral content (BMC), bone volume, and bone mineral density (BMD), were significantly lower in the DEX-treated group than in the control group. Furthermore, lower BMC and BMD in the DEX-treated group were associated with impaired bone-related gene expression, as reflected by the weaker expression of Runx2, osterix (Osx), alkaline phosphatase (ALP), and osteopontin (OPN) than that in the control group. On the other hand, significantly higher total and cancellous BMD were observed in the LF-treated group than in the DEX-treated group. Furthermore, Osx and ALP gene expression was significantly stronger in the LF-treated group than in the DEX-treated group. These results suggest that the treatment with LF prevented DEX-induced osteoporosis in mice.