Fig. 4

Aspirin inhibits RANKL-induced OCs via the IκK/IκB/NF-κB pathway. a, b Western blot showing that RANKL treatment upregulated IKK, p-IKK, IKB, p-IKB, and p-p65 and that IKK inhibitor treatment significantly reduced this upregulation. The expression levels of NFATc1 showed the same tendency. c Components of the IκK/IκB/NF-κB pathway were overexpressed after RANKL induction, which was decreased by aspirin pretreatment, with the results for NFATc1 expression being consistent. d Schematic representation of the timing of aspirin and IKK inhibitor treatment in our experiments. e Based on all of the results described above, aspirin inhibits RANKL-induced OCs via the NF-κB pathway, ultimately suppressing NFATc1 synthesis. All experiments are representative of at least three replicates