Research Paper Volume 15, Issue 19 pp 10705—10731

Figure 5. Silencing of cGlra2 protects against oxidative stress-induced RGC injury. (A) RGCs were transfected with scrambled (Scr) siRNA, cGlra2 siRNA, or left untreated (Ctrl) for 24 h. qRT-PCRs were conducted to examine the expression of cGlra2 (n = 4). (B) RGCs were transfected with scrambled (Scr) siRNA, cGlra2 siRNA, or left untreated (Ctrl) for 24 h. CCK-8 assays were performed to detect RGC viability (n = 4). (C–G) RGCs were transfected with Scr siRNA, cGlra2 siRNA, or left untreated (Ctrl) for 12 h and then exposed to H₂O₂ (100 μmol/L) to mimic oxidative stress for additional 36 h. CCK-8 assays were performed to detect RGC viability (C, n = 4). Hoechst staining and quantification analysis were performed to detect the changes of nuclei morphological characteristics of RGCs (D and E, n = 4, Scale bar: 50 μm). JC-1 staining was performed to detect the change of mitochondrial depolarization in RGCs (F, n = 4, Scale bar: 50 μm). Caspase 3/7 activity was performed to detect the degree of RGC apoptosis (G, n = 4). ^*P < 0.05 vs. Ctrl group; ^#P < 0.05 between the marked groups. All significance was examined using One-way ANOVA followed by Bonferroni’s post hoc test.