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 6
NGR2-mediated activation of P90RSK and Nrf2 was dependent of MEK1/2-ERK1/2 pathways but independent on JNK, P38, or PI3K/Akt pathways. The expression of proteins was determined by western blot analysis. The SH-SY5Y cells were preincubated with different inhibitors for 1 h followed by treatment with 20 μM NGR2 for 24 h. (a) NGR2-mediated the phosphorylation of P90RSK and the nuclear Nrf2 accumulation were effectively prevented by MEK inhibitor PD98059 but not by JNK inhibitor SP600125, p38 inhibitor SB203580, or PI3K/Akt inhibitor LY294002. (b) Treatment of SH-SY5Y cells with 20 μM NGR2 for different periods of time (4, 8, 16, 24 h) resulted in the activation of MEK1/2-ERK1/2 pathways.
