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. 2018 Mar 27;9:210. doi: 10.3389/fphar.2018.00210

Figure 5.

Figure 5

CEP suppressed RANKL-induced activation of the JNK and AKT pathways in vitro. (A) BMMs were cultured in osteoclastogenic medium with or without CEP treatment for 0, 1, 2, and 3 days. Cell lysates of samples from day 0 to day 3 were collected and analyzed by Western blotting using specific antibodies against NFATc1, c-Fos, and CatK. (B) The gray levels of NFATc1, c-Fos, and CatK were analyzed by normalization to α-tubulin. (C) After culture for 3 days, the cells were collected and the mRNA expression levels of NFATc1 and c-Fos were analyzed. (D) BMMs were pre-treated with or without CEP for 2 h and were subsequently treated with RANKL for 0, 5, 10, 20, 30, and 60 min. Cells were collected and lysates were analyzed by Western blotting using primary antibodies specific to p-p65, p65, p-ERK1/2, ERK, p-JNK1/2, JNK1/2, p-p38, p38, p-IκBα, IκBα, p-AKT, AKT, p-PI3K, PI3K, and α-tubulin. (E,F) The gray levels of p-JNK1/2, p-AKT, and p-PI3K were analyzed by normalization to total JNK1/2, AKT, and PI3K. Values are expressed as mean ± SD; *P < 0.05, **P < 0.01 vs. the control group.