Fig 1: Ferulic acid, pterostilbene, and tyrosol modulate PERK pathway activation in response to severe ER stress. H9c2 cells were pre-treated for 1 h with ferulic acid (FrA, 5 µM), pterostilbene (Pts, 0.5 µM), or tyrosol (Tyr, 1 µM) and then were treated for 6 h with tunicamycin (TN, 10 µg/mL), and the relative mRNA levels of PERK pathway genes ATF4 (A, n = 4) and GADD34 (B, n = 5) were quantified by qPCR. The phosphorylation of the translation initiation factor eIF2a was analyzed by western blot after 1h30 treatment with TN ± phenolic compounds. Representative western blots under ferulic acid (C), pterostilbene (D), or tyrosol (E) treatment are presented. Bar graphs show the ratios of phosphorylated vs. total eIF2a (F–H, n = 4). The mRNA and protein levels of the pro-apoptotic factor CHOP were analyzed in response to TN with or without phenolic compounds (I–M, n = 5). Actin was used as a loading control. Values in the bar graphs represent mean ± S.E.M. * p < 0.05, ** p < 0.01 *** p < 0.001 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. TN.