Paeoniflorin Inhibits Receptor Activator for Nuclear FactorκB (RANK) Ligand-Induced Osteoclast Differentiation In Vitro and Particle-Induced Osteolysis In Vivo.
Med Sci Monit. 2018 Feb 20 ;24:1044-1053. Epub 2018 Feb 20. PMID: 29459582
BACKGROUND Paeoniflorin (PF), a glucoside isolated from the dried root of Paeonia lactiflora Pall, has been reported to have a number of pharmacological properties, including immunity-regulation, anticancer activities, and neuroprotective effect. However, PF's pharmacological role in bone disorder has been seldom reported. Hence, this study was designed to investigate the effects of PF on osteoclast differentiation and osteolysis diseases. MATERIAL AND METHODS The bone marrow macrophages were isolated from C57BL/6 mice and incubated with RANK ligand (RANKL) and various concentrations of PF. After 5 days of incubation, tartrate-resistant acid phosphatase (+) cells and bone resorption pits were counted. Effects of PF on expression of osteoclast-specific protein and gene were investigated via Western blot, q-PCR, and immunofluorescence assay. The osteoprotective effect of PF in vivo was evaluated in a calvarial osteolysis model via micro-CT scan and histological stain. RESULTS In vitro, PF intervention inhibited osteoclast formation and resorption activity. PF also impaired RANKL-induced NF-κB phosphorylation and immigration to the nucleus. PF suppressed osteoclast-marker protein and gene expression. In vivo, PF inhibited cobalt-chromium-molybdenum alloy particle-induced osteolysis and reduced osteoclast number in tissue slice. CONCLUSIONS PF is a potential agent against osteolysis-related diseases caused by excessive osteoclast activity.