Research Paper Volume 15, Issue 19 pp 10705—10731

Figure 6. Silencing of cGlra2 protects against hydrostatic stress-induced RGC injury. RGCs were maintained under the elevated hydrostatic pressure (70 mm Hg) to induce hydrostatic stress. RGCs maintained at the ambient pressure were taken as the control group. RGCs were transfected with Scr siRNA, cGlra2 siRNA, or left untreated (Ctrl) for 12 h, and then accepted hydrostatic stress for additional 36 h. CCK-8 assays were performed to detect the viability of RGCs (A, n = 4). Hoechst staining and quantification analysis was performed to detect the changes of nuclei morphological characteristics of RGCs (B and C, n = 4, Scale bar: 50 μm). JC-1 staining was performed to change of mitochondrial depolarization in RGCs (D, n = 4, Scale bar: 50 μm). Caspase 3/7 activity was performed to detect the degree of RGC apoptosis (E, n = 4). ^*P < 0.05 vs. Ctrl group; ^#P < 0.05 between the marked groups. All significance was examined using the One-way ANOVA followed by Bonferroni’s post hoc test.