Vancomycin is an effective
antibiotic for treatment of bone
infection caused by Staphylococcus aureus, however, a high local concentration of
vancomycin might induce a delay in bone union.
Icariin has been reported to suppress osteoclastogenes and promote osteogenesis. Our study aimed to investigate the effect of
icariin on bone repair after anti-
infection treatment in vivo and to explore the resisting effect of
icariin on rat calvarial osteoblasts (ROBs) inhibited with high doses of
vancomycin. Rabbits with bone
infection of S. aureus were treated with implanted
vancomycin-
calcium sulfate (VCS) and
icariin at 10.86 mg/kg/day for consecutive 8 weeks. Micro-CT, morphology, blood biochemistry were evaluated. In addition, ROBs were treated with
vancomycin and
icariin at different doses. Cell proliferation and differentiation capabilities, BMP2, Runx2, OPG, RANKL
mRNA levels and
protein expression were assessed. The results indicated that high dose of
vancomycin significantly decreased bone mass and inhibited
osteocalcin secretion;
icariin increased these indicators compared with the single
vancomycin treatment. Over 0.1 mg/mL of
vancomycin inhibited the proliferation and differentiation of ROBs, while
icariin resisted the inhibition of
vancomycin by regulating cell cycle and promoting the
Alkaline phosphatase (ALP) activity. Moreover,
icariin promote bone formation by up-regulating BMP2/Runx2 and OPG/RANKL pathways.
Icariin exhibited osteoplastic properties on osteoblasts that had been inhibited with high doses of
vancomycin. Therefore,
icariin is helpful for post-
infection treatment of bone
infection.