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. 2020 Sep 15;37:101728. doi: 10.1016/j.redox.2020.101728

Fig. 7.

Fig. 7

PCB2 increased AMPK phosphorylation via PPARδ activation. (A) HUVECs were exposed to PCB2 (10 μM) for indicated time periods. Phosphorylated-AMPK and AMPK levels were detected. (B) Quantification of p-AMPK/AMPK level as in (A) (n = 3). All data were expressed as mean ± SEM. **P < 0.01 vs. vehicle. (C) HUVECs were treated with GSK0660 (1 μM) for 1 h before the exposure to PCB2 (10 μM) for 6 h, the levels of p-AMPK and AMPK were detected. (D) Quantification of p-AMPK/AMPK level as in (C) (n = 3). All data were expressed as mean ± SEM. *P < 0.05 vs. vehicle; ##P < 0.01 vs. PCB2. (E) HUVECs were pretreated with GSK0660 (1 μM, 1 h) and, then, incubated with PCB2 (10 μM, 12 h) before the exposure to HG (30 mM, 24 h). Protein levels of p-AMPK and AMPK were measured. (F) Quantification of p-AMPK/AMPK level as in (E) (n = 3). All data were expressed as mean ± SEM. *P < 0.05, **P < 0.01 vs. vehicle; ##P < 0.01 vs. HG; †P < 0.05 vs. PCB2+HG.