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. 2018 Feb 14;16:47–58. doi: 10.1016/j.redox.2018.02.008

Fig. 7.

Fig. 7

PKA signaling involved in the effects of FCPR16 towards MPP+-induced deficits in mitochondrial membrane potential (Δψm) and oxidative damage. (A) SH-SY5Y cells were pretreated with 10 μM H-89 for 1 h before FCPR16 treatment for 1 h, and then incubated with or without 500 μM MPP+ for another 24 h. Δψm was determined by JC-1 assay. Bar= 100 µm. (B) Quantitive data of A. (C) SH-SY5Y cells were pretreated with 10 μM H-89 for 1 h before FCPR16 treatment for 1 h, and then incubated with or without 500 μM MPP+ for another 2 h. ROS level was determined using DCFH-DA as a molecular probe. Bar = 100 µm. (D) Quantitive data of C. (E) SH-SY5Y cells were pretreated with 10 μM H-89 for 1 h before FCPR16 treatment for 1 h, and then incubated with or without 500 μM MPP+ for another 48 h. Cell viability were measured by CCK-8 assay. ###P < 0.001 compared with control; *P < 0.05, * *P < 0.01 compared with MPP+; $$P < 0.01, compared with (FCPR16 + MPP+) treated group.