Skip to main content
. 2017 Nov 30;24(4):207–215. doi: 10.11005/jbm.2017.24.4.207

Fig. 3. Fexaramine (Fexa) inhibits receptor activator of nuclear factor-κB ligand (RANKL)-induced expression of c-Fos and nuclear factor of activated T cells (NFATc1). (A, B) Bone marrow-derived macrophages (BMMs) were preincubated in the absence or presence of fexa (5 µM) for 30 min, and then treated with or without 200 ng/mL of RANKL for 24 hr. Cell lysates were then subjected to Western blot analysis using (A) NFATc1 or (B) c-Fos antibodies. (C) BMMs were infected through the retrovirus packaging system. Infected BMMs were cultured with RANKL (100 ng/mL) and macrophage-colony stimulating factor (30 ng/mL) in the absence or presence of fexa (5 µM) for 4 days. The recovery rate was defined as the percentage of osteoclast formation in the presence of fexa. The osteoclast formation in the presence of vehicle was given as 100%. Data are expressed as mean±standard deviation from at least three independent experiments. *P<0.05. Veh, vehicle.

Fig. 3