Original Article
Background: To determine the osteoclastogenesis inhibitory e ect and inside mechanisms of a curcuminoids-rich extract (CRE) and three water-soluble CREs, namely CRE-SD (CRE in solid dispersion form), CRE-Bin (CRE binary complex with hydroxypropyl-β-cyclodextrin), and CRE-Ter (CRE ternary complex with hydroxypropyl-β-cyclodextrin and polyvinylpyrrolidone K30), as well as curcumin (Cu), bisdemethoxycurcumin (Bis), and demethoxycurcumin (De). Methods: TRAP (tartrate-resistant acid phosphatase) and acid phosphatase assays were used to con rm osteoclastogenesis. MTT [(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, a tetrazole] and LDH (lactate dehydrogenase) assays were performed to evaluate cell viability and cell cytotoxicity, respectively. Mechanisms of action and signaling pathways were explored using Western blot analysis. Bone degradation was measured using a bone pit and uorescein assays. Results: A reduction in both TRAP content was demonstrated, along with lower levels of the osteoclast-speci c genes cathepsin K, c-Fos, and NFATc1 (Nuclear factor of activated T cells 1), as a consequence of the e ects of CRE-Ter, CRE-Bin, CRE-SD, CRE, and Cu. Exposure to CRE-Ter, CRE-Bin, and CRE-SD at 20 µg/ml and CRE and curcumin at 5 µg/ml, respectively, prevented multinuclear formation, increased acid phosphatase granule content, and reduced TRAP activity in RANKL (receptor activator of nuclear factor к-B ligand)-treated RAW 264.7 cells. Furthermore, all curcuminoids could suppress the canonical RANKL-induced NF-кB (nuclear factor kappa B) pathway component, p-NF-кB p65 protein, while the bone pit assay con rmed that bone degradation could be reduced by curcuminoids, while the cell uorescence content could also be lowered. Conclusion: It was determined through the tests carried out in this research that the principal inhibitors of bone resorption and osteoclastogenesis were CRE-Ter, CRE-Bin, CRE- SD, CRE, and Cu.
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