P90RSK and Nrf2 Activation via MEK1/2-ERK1/2 Pathways Mediated by Notoginsenoside R2 to Prevent 6-Hydroxydopamine-Induced Apoptotic Death in SH-SY5Y Cells
Figure 5
NGR2 reversal of 6-OHDA-induced oxidative stress, mitochondrial membrane depolarization, and apoptosis-related protein deregulation in SH-SY5Y cells. The SH-SY5Y cells were preincubated with 20 μM NGR2 for 24 h followed by treatment with 50 μM 6-OHDA for 24 h. (a) NGR2 reversal of 6-OHDA induced the increase in MDA production and ROS generation, as well as the decrease of nuclear Nrf2, HO-1, GSH-PX, and GR activities in SH-SY5Y cells. (b) NGR2 reversal of mitochondrial membrane depolarization. (c) The cells labeled by JC-1 were analyzed by a high content screening system. (d) NGR2 suppression of 6-OHDA induced increase in cytochrome c release, upregulation of cleaved caspase-9 and cleaved caspase-3, and downregulation of p-BAD. The results are expressed as the mean ± SD of three independent experiments. ## indicates a significant difference from the control (). ** indicates a significant difference from the 6-OHDA treatment alone ().
