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.