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. 2017 Nov 23;7:16158. doi: 10.1038/s41598-017-16488-x

Figure 3.

Figure 3

Liraglutide ameliorates the ectopic expression of pro-apoptotic UPR mediators and promotes ER proteostasis in the neuroblastoma SH-SY5Y cell line upon persistent ER stress. Twenty-four hours post seeding, SH-SY5Y cells were serum starved for 8 h and treated with 0 or 100 nM of thapsigargin for 16 h, in the presence or absence of 100 nM Liraglutide. Cells were harvested, and the expression of CHOP [(a)], caspase 12 (CASP12) [(b)], ER oxidoreductase 1 alpha (Ero1-Lα) [(c)], protein disulfide isomerase [PDI; (d)] and of calnexin [(e)] were determined by western blotting. β-Actin was used as the loading control to all western blot analyses. Each bar represents mean ± SEM from four independent experiments. Data is expressed as fold change to the control (CNTRL; unstressed/untreated conditions). Data was analysed by one- and two-way ANOVA, followed by post hoc Bonferroni’s multiple comparison t-test (* p ≤ 0.05, ** p ≤ 0.01 & *** p ≤ 0.001 compared to CNTRL; # p ≤ 0.05, ## p ≤ 0.01 & ### p ≤ 0.001 compared to the corresponding thapsigargin-treated cells).