Figure 5 of Lee, Mol Vis 2012; 18:838-850.

Figure 5. Advanced glycation end products–BSA (AGE-BSA) treatment induces c-Jun N-terminal kinase (JNK)2/3, and JNK2/3 induction is reversed by a high-mobility group box protein 1 (HMGB1) blocker. A: The phosphorylations of JNK, extracellular-signal-regulated kinase (ERK), and p38 in mitogen-activated protein kinase (MAPK) signaling in retinal ganglion cell (RGC)-5 cells treated with 200 μg/ml of AGE-BSA for more than 3 h were detected by western blot analysis. Only phospho-JNK2/3, but not phospho-ERK or phospho-p38, significantly increased at 3 h after treatment with AGE-BSA compared with the BSA control (n=4). B: Glycyrrhizin (100 μM), SP600125 (10 μM), and NAC (10 mM) decreased AGEs-induced upregulation of phospho-JNK2/3 (n=4). C: Treatment with GZ and NAC for 24 h showed insignificant changes relative to sterile PBS in cell viabilities of RGC-5 assayed with XTT (n=6). Abbreviations: A, AGE-BSA; B, BSA; G50 and G100, glycyrrhizin at 50 and 100 μM; SP, SP600125; N5 and N10, NAC at 5 and 10 mM.