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. 2017 Feb 3;39(3):539–548. doi: 10.3892/ijmm.2017.2876

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Copyright: © Choe et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Melittin influencea osteoclast formation in time- and dose-dependent manner. (A) Osteoclastogenic genes, such as TRAP, cathepsin K, matrix metalloproteinase-9 (MMP-9) and carbonic anhydrase II, in the course of osteoclastogenesis in RAW 264.7 cells incubated with receptor activator of nuclear factor-κB ligand (RANKL) (50 ng/ml) for 0, 3, 5, 7, 9 and 11 days were measured (^*p<0.001, ^**p<0.01 and ^†p<0.05 compared to non-treated cells). (B) Melittin (1 µg/ml) was added to the RAW 264.7 cells on days 3 and 5 following stimulation with RANKL. Inhibitory effect of melittin (1 µg/ml) treatment for 0, 3 and 5 days on osteoclastogenic genes was assessed (^*p<0.01 and ^**p<0.001 compared to RANKL-stimulated cells without melittin). (C) RAW 264.7 cells treated with RANKL (50 ng/ml) were cultured at different dosages of melittin (0.2 to 1.0 µg/ml) (^*p<0.05 and ^**p<0.01 compared to non-treated cells). (D) Melittin was added to the RAW 264.7 cells on days 3 and/or 5 following stimulation with RANKL. The in vitro morphological and functional analyses for osteoclastogenesis were performed using TRAP staining, pit formation, and F-actin ring staining assays in RAW 264.7 cells treated with RANKL with or without melittin (^*p<0.01 compared to non-treated cells) (E) The assessment of osteoclast-like cells differentiated from bone marrow-derived macrophages (BMMs) was done using TRAP staining and F-actin ring staining assays. Data are representative of 3 independent experiments.

Melittin influencea osteoclast formation in time- and dose-dependent manner. (A) Osteoclastogenic genes, such as TRAP, cathepsin K, matrix metalloproteinase-9 (MMP-9) and carbonic anhydrase II, in the course of osteoclastogenesis in RAW 264.7 cells incubated with receptor activator of nuclear factor-κB ligand (RANKL) (50 ng/ml) for 0, 3, 5, 7, 9 and 11 days were measured (^*p<0.001, ^**p<0.01 and ^†p<0.05 compared to non-treated cells). (B) Melittin (1 µg/ml) was added to the RAW 264.7 cells on days 3 and 5 following stimulation with RANKL. Inhibitory effect of melittin (1 µg/ml) treatment for 0, 3 and 5 days on osteoclastogenic genes was assessed (^*p<0.01 and ^**p<0.001 compared to RANKL-stimulated cells without melittin). (C) RAW 264.7 cells treated with RANKL (50 ng/ml) were cultured at different dosages of melittin (0.2 to 1.0 µg/ml) (^*p<0.05 and ^**p<0.01 compared to non-treated cells). (D) Melittin was added to the RAW 264.7 cells on days 3 and/or 5 following stimulation with RANKL. The in vitro morphological and functional analyses for osteoclastogenesis were performed using TRAP staining, pit formation, and F-actin ring staining assays in RAW 264.7 cells treated with RANKL with or without melittin (^*p<0.01 compared to non-treated cells) (E) The assessment of osteoclast-like cells differentiated from bone marrow-derived macrophages (BMMs) was done using TRAP staining and F-actin ring staining assays. Data are representative of 3 independent experiments.