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

Figure 2

IRF9 reversed cell apoptosis inhibited 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 and b) The protein level of IRF9 was tested by Western blot analysis. β-actin is a loading control.  < 0.05 vs. pcDNA-NC. (c and d) The cell apoptosis was assessed by Annexin V FITC/PI staining flow cytometry. (e–k) The expression of Bcl-2, Cleaved-Caspase 3, Bax, AIF, and cytochrome C was determined by Western blot analysis. β-actin is a loading control.  < 0.01 vs. control group,  < 0.001 vs. control group, ^# < 0.05 vs. MPP⁺-treated group, ^## < 0.01 vs. MPP⁺-treated group, ^& < 0.05 vs. MPP⁺ + miR-20a-5p mimic-cotreated group, ^$ < 0.05 vs. MPP⁺ + pcDNA-IRF9-cotreated group, and ^$$ < 0.01 vs. MPP⁺ + pcDNA-IRF9-cotreated group. Data are expressed as mean ± SD. The experiments were repeated six times.

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