Figure 5 of Biermann, Mol Vis 2011; 17:1275-1286.


Figure 5. Hydrogen sulfide–induced differential mitogen-activated protein kinase regulation in the retina. Effect of hydrogen sulfide (H2S) preconditioning on mitogen-activated protein kinases (MAPKs) phosphorylated (p)- extracellular signal-regulated kinase (ERK)1/2 (A), p- c-jun N-terminal kinase (JNK; B), and p-p38 (C) 24 h after unilateral ischemia. MAPK levels were determined using specific antibodies. The histograms represent the densitometric ratio of MAPKs compared with its nonphosphorylated form, total (t)ERK1/2, JNK, or p38. A: p-ERK1/2 is suppressed through inhalational H2S preconditioning. While p-ERK was baseline activated in the nonpretreated animals (control and ischemia/reperfusion [I/R] injury), H2S significantly inhibited ERK1/2 phosphorylation in both control and ischemic retinas (fourfold reduction in H2S + I/R injury versus I/R injury; *p<0.05). B: I/R injury per se significantly increased the phosphorylation of the JNK (3.8-fold induction in I/R injury versus control; p<0.001). Again, preconditioning with inhalative H2S inhibited JNK phosphorylation completely (3.7-fold reduction in H2S + I/R injury versus I/R injury; ***p<0.001). C: The phosphorylation of p38 MAPK was comparable in all groups without significant differences. Data are presented as mean±SD of eight experiments.