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. 2018 Mar 5;9(6):568–579. doi: 10.1007/s13238-018-0513-z

Figure 3.

Figure 3

G-Rg5 and G-Rk1 inhibited NF-κB activation and down-regulated downstream anti-apoptosis genes. (A) NF-κB activity was examined by luciferase reporter assay under treatment with G-Rg5 (6 μmol/L), G-Rk1 (6 μmol/L), etoposide (25 μg/mL) and PMA (100 ng/mL). (B–F) Relative gene expression levels of IL-6 (B), X-IAP (C), c-IAP1 (D), c-IAP2 (E) and survivin (F) were examined by qRT-PCR under treatment with G-Rg5 (6 μmol/L), G-Rk1 (6 μmol/L), etoposide (25 μg/mL) and PMA (100 ng/mL). (G) Protein levels of X-IAP, c-IAP1, c-IAP2 and survivin were examined by immunoblot under treatment with G-Rg5 (6 μmol/L), G-Rk1 (6 μmol/L), etoposide (25 μg/mL) and PMA (100 ng/mL), and β-actin was shown as a loading control. All data are shown as the mean ± SD and the experimental points show the average of at least triplicates. All experiments were repeated at least 3 times