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. Author manuscript; available in PMC: 2016 Dec 15.

Published in final edited form as: Eur J Pharmacol. 2015 Nov 10;769:100–109. doi: 10.1016/j.ejphar.2015.11.003

Fig. 4 — RAW264.7 cells were plated on to Bone Resorption Assay Kit 48 plates and cultured in differentiation medium without (control) or with Br-H A (0.1 and 0.5 μg/ml) for 6 days. (A) A microscopic photograph of a CaP coated plate (on day 6), without RANKL, with RANKL only (100 ng/ml), and with RANKL and Br-H A (0.1 and 0.5 μg/ml) respectively. (B) The inhibitory effects of Br-H A on the resorption of CaP induced by RANKL (100 ng/ml) were evaluated by fluorescence intensity. (C) The histogram represents the relative pit area (%) compared with that of the control (#). The results are expressed as mean ± S.D. of triplicate experiments. *P<0.05 indicates significant differences from the RANKL stimulated group.

Fig. 4 — RAW264.7 cells were plated on to Bone Resorption Assay Kit 48 plates and cultured in differentiation medium without (control) or with Br-H A (0.1 and 0.5 μg/ml) for 6 days. (A) A microscopic photograph of a CaP coated plate (on day 6), without RANKL, with RANKL only (100 ng/ml), and with RANKL and Br-H A (0.1 and 0.5 μg/ml) respectively. (B) The inhibitory effects of Br-H A on the resorption of CaP induced by RANKL (100 ng/ml) were evaluated by fluorescence intensity. (C) The histogram represents the relative pit area (%) compared with that of the control (#). The results are expressed as mean ± S.D. of triplicate experiments. *P<0.05 indicates significant differences from the RANKL stimulated group.