Crocin inhibits RANKL-induced osteoclast formation and bone resorption by suppressing NF-κB signaling pathway activation

Abstract

Crocin is a dietary compound with antioxidant and anti-inflammatory properties, but its effects on bone resorption have not been well characterized. Here we address this issue by examining the direct effects of crocin on osteoclast cells in vitro. Osteoclastogenesis was induced by RANKL (receptor activator of NF-κB ligand) in mouse bone marrow-derived macrophages in the absence or presence of crocin at various concentrations. Further, the bone resorption activity of mature osteoclast treated with crocin was assessed by pit assay. Without altering cell viability, crocin was shown to inhibit the differentiation and function of osteoclast cells in a dose-dependent manner. Mechanistically, RANKL-induced NF-κB and NFATc1 activation, the critical signaling pathways for osteoclast differentiation and function, were both repressed by crocin in bone marrow-derived macrophages. Thus, crocin suppresses osteoclastogenesis through direct inhibition of intracellular molecular pathways, which may contribute to future development of anti-bone resorption treatment.