Research Paper Volume 14, Issue 12 pp 5177—5194

Figure 6. Inhibition of PEG11as alleviated OGD/R-induced apoptosis by ameliorating autophagic flux defects via miR-874-3p/ATG16L1 axis in N2a cells. (A) PEG11as silencing down-regulated ATG16L1 expression in tMCAO/R mice after transfection with sh-PEG11as. n = 6 animals/group. (B) PEG11as regulated ATG16L1 expression by sponging miR-874-3p. The cells were transfection with sh-PEG11as or co-treated with miR-874-3p inhibitor. 48 hours later, the cells were exposed to OGD 4 hours and 24 hours of Reperfusion in N2a cells. n = 3. (C, D) Knockdown of ATG16L1 ameliorate OGD/R-induced autophagic flux defects. (E) LC3-II/LC3-I ratio and p62 level were determined by western blot after transfection of ATG16L1 siRNA in N2a cells exposed to OGD/R. (F, G) TUNEL staining for analysis of the cell apoptosis after treated with 3-MA, sh-PEG11as or sh-ATG16L1, respectively. n = 3. One-way ANOVA followed by the Tukey’s post-hoc-test was used, data are shown as mean ± SD. Data are statistically different from each other with ^*P < 0.05, ^**P < 0.01, and ^***P < 0.001.