Abstract
Osteolytic skeletal disorders are caused by an imbalance in the osteoclast and osteoblast function. Suppressing the differentiation and resorptive function of osteoclast is a key strategy for treating osteolytic diseases. Dracorhodin perchlorate (D.P), an active component from dragon blood resin, has been used for facilitating wound healing and anti‐cancer treatments. In this study, we determined the effect of D.P on osteoclast differentiation and function. We have found that D.P inhibited RANKL‐induced osteoclast formation and resorbed pits of hydroxyapatite‐coated plate in a dose‐dependent manner. D.P also disrupted the formation of intact actin‐rich podosome structures in mature osteoclasts and inhibited osteoclast‐specific gene and protein expressions. Further, D.P was able to suppress RANKL‐activated JNK, NF‐κB and Ca2+ signalling pathways and reduces the expression level of NFATc1 as well as the nucleus translocation of NFATc1. Overall, these results indicated a potential therapeutic effect of D.P on osteoclast‐related conditions.
Highlights
To determine the effect of D.P on receptor activated nuclear factor kappa-B ligand (RANKL)-induced osteoclast formation, Bone marrow macrophages (BMMs) were seeded onto 96-well plates and RANKL was added with or without the presence of Dracorhodin perchlorate (DP) It was observed in the RANKL control group that tartrate-resistant acid phosphatase (TRAcP)-positive multinucleated cells appeared after the stimulation with RANKL
Further to the calcium oscillation, it was found by real-time PCR that the gene expression levels of Ctr and Nfatc[1] during RANKL-induced osteoclastogenesis were suppressed by D.P (Figure 6B)
We have demonstrated its inhibitory effects on osteoclast formation and function
Summary
For the study of osteoclast-specific protein expression, the BMMs were seeded into 6-well plates at a density of 1 × 105 cells/well and stimulated with RANKL (50 ng/mL) and in the presence or absence of D.P (30 μmol/L) for 0, 1, 3 and 5 days separately.
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