MiR-20a-5p Regulates MPP⁺-Induced Oxidative Stress and Neuroinflammation in HT22 Cells by Targeting IRF9/NF-κB Axis

Figure 3

IRF9 offset mitochondrial dysfunction attenuated by miR-20a-5p overexpression in MPP⁺-treated HT22 cells. HT22 cells were pretreated with miR-20a-5p mimic and/or pcDNA-IRF9 for 24 h and then treated with MPP⁺ (0.5 mM) for 24 h. (a) Reactive oxygen species (ROS) activity was performed using DCFH-DA. (b) The mitochondrial membrane potential (MMP) was assayed by JC-1 fluorescent probe. The contents of SOD, GSH-XP, and MDA in cells (c–e) and supernatant (f–h) were tested by enzyme-linked immunosorbent assay (ELISA).  < 0.01 vs. control group,  < 0.001 vs. control group, ^# < 0.05 vs. MPP⁺-treated group, ^## < 0.01 vs. MPP⁺-treated group, ^### < 0.001 vs. MPP⁺-treated group, ^& < 0.05 vs. MPP⁺ + miR-20a-5p mimic-cotreated group, ^&&& < 0.001 vs. MPP⁺ + miR-20a-5p mimic-cotreated group, ^$ < 0.05 vs. MPP⁺ + pcDNA-IRF9-cotreated group, ^$$ < 0.01 vs. MPP⁺ + pcDNA-IRF9-cotreated group, and ^$$$ < 0.001 vs. MPP⁺ + pcDNA-IRF9-cotreated group. Data are expressed as mean ± SD. The experiments were repeated six times.

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