Figure 7

ROS production in response to propofol treatment is reduced in RCC4-EV cells. (a and b) RCC4-EV cells were transfected with small interfering RNA (siRNA) targeting pyruvate dehydrogenase kinases 1 (PDK-1) or a negative control (scr). Cells were exposed to 50 µM propofol and ROS generation (a) and caspase 3/7 (b) were assayed. (c) ROS generation in RCC4-VHL cells and RCC4-EV cells exposed to 50 µM propofol (n = 3) were assayed. (d and e) RCC4-EV (d) and RCC4-VHL (e) cells were exposed to 50 µM propofol for 6 h with or without 10 mM NAC treatment. Caspase 3/7 activity of the cells were assayed. Differences were evaluated by two-way ANOVA followed by Dunnett’s test for multiple comparisons; *p < 0.05, as compared to the control cells (no treatment); ^#p < 0.05 for the indicated comparison. (f and g) RNA-seq analysis of the expression levels of selected genes within (f) GO:0016909 (antioxidant activity) and (g) GO:1903426-8 (regulation of reactive oxygen species biosynthetic process) in RCC4-EV and RCC4-VHL cells. The y axis indicates the ratio of the average FPKM values for RCC4-VHL cells.