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. 2017 Jan 5;11:524–534. doi: 10.1016/j.redox.2016.12.036

Fig. 3.

Fig. 3

NOX4 played dual roles in endothelial apoptosis induced by t-BHPL NOX4 was knocked down by siNOX4 (A), inhibited by GKT137831 (10 nM) (B), or overexpressed by NOX4 plasmid (over-NOX4) (F), the ROS production (C, D, and G) and the caspase 3/7 activities (E and H) in response to t-BHPL were determined. The Akt and p-Akt protein expression in normal (I) and NOX4 overexpressed (J) cells in response to t-BHPL were determined by Western blotting. NOX4 overexpressed cells were treated with t-BHPL for 1 h with or without Akt inhibitor VIII (5 μM) pretreatment for 1 h and the caspase 3/7 activities were detected by caspase 3/7 Activity Assay Kit (K). The results were expressed as mean±SD of three independent experiments. ROS, reactive oxygen species; Cont, control group.