Skip to main content
. 2017 Sep 11;18(9):1945. doi: 10.3390/ijms18091945

Figure 5.

Figure 5

ROS production is upstream of JNK pathway activation and Akt-mTOR pathway inhibition in SH-mediated autophagy (A) Effects of IGF-1 and SP600125 on SH-induced ROS generation in U87 and SF767 cells. The cells were exposed to SH (0.5 mM) in the absence or presence of IGF-1 or SP600125 for 24 h, and intracellular ROS levels were investigated using DCFH-DA probes, with the resulting fluorescence being read by a fluorescence microplate reader; (B) Effects of NAC on SH-mediated Akt-mTOR pathway inhibition and JNK pathway activation in U87 and SF767 cells. The cells were treated with SH (0.5 mM) for 24 h in the absence or presence of NAC. β-actin was used as the loading control. All blots shown are representative of n = 3 experiments, with similar results. Data are expressed as the mean ± SEM, n = 3. ** p < 0.01, versus the control. NS, not significant versus the group treated with SH alone.