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.