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. Author manuscript; available in PMC: 2022 Feb 1.
Published in final edited form as: Cell Signal. 2020 Nov 24;78:109847. doi: 10.1016/j.cellsig.2020.109847

Fig. 5. Activation of AC/PKA partly abolishes DA’s anti-osteoclastogenic effect.

Fig. 5.

RAW cells were treated with vehicle (Ctrl), 100 μM DA, 10 μM AC agonist Forskolin, or 50 μM PKA agonist 8-Br-cAMP as indicated, in the presence of 10 ng/mL RANKL for 3 days. (A, B) Western blot detection of p-CREB/CREB. (C) For p-CREB luciferase activity assay, p-CREB-Luc reporter-transfected RAW cells were used to receive the treatment same as above. (D) TRAP staining and quantification of OCs. TRAP positive, multinucleated OC in red were counted. Scale bar is 200μm. (E) RT-qPCR detection of osteoclastic genes (c-Fos, Nfatc1, Trap, Ctsk); normalized to B2m. n=3 for all experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs. Ctrl group; *P < 0.05, ##P < 0.01, ###P < 0.001 vs. DA group. Data shown as mean ± SEM.