Figure 5.

Trx-TrxR system regulates the denitrosylation of procaspase-3 as well as its activation during I/R in hippocampus. (a) Time course analysis of FasL levels in hippocampal CA1 derived from sham-treated rats or rats with 15 min ischemia at various time points (1, 2, 3, 6, and 12 h) after reperfusion (R). n=4; *P<0.05 compared with sham group. (b) Auranofin protected S-nitrosylation of procaspase-3 after 3 h reperfusion. Auranofin (10 mM), an inhibitor of TrxR, was administrated 30 min before ischemia. The samples were processed using the biotin switch method followed by western blotting. n=4; *P<0.05 compared with sham group, ^#P<0.05 compared with DMSO group. (c) Auranofin inhibited procaspase-3 activation after 6 h reperfusion (n=4; *P<0.05 compared with corresponding sham group, ^#P<0.05 compared with corresponding DMSO group). (d) TrxR2 AS-ODNs (AS) affects TrxR2 expression in sham rats. 10 nmol TrxR2 AS-ODNs, sense-ODNs control (sense), or vehicle (TE) was administrated to the rats every 24 h for 3 days. TrxR2 AS significantly decreased TrxR2 expression, whereas sense-ODNs had no effect (n=4; *P<0.05 compared with TE group). (e) TrxR2 AS-ODNs decreased TrxR2 expression during I/R. 10 nmol TrxR2 AS, sense control (sense), or vehicle (TE) was administrated to the rats every 24 h for 3 days before ischemia. After 6 h reperfusion, TrxR2 AS decreased TrxR2 expression, whereas sense-ODNs had no effect (n=4; *P<0.05 compared with sham group, ^#P<0.05 compared with TE group). (f) TrxR2 AS-ODNs protected S-nitrosylation of procaspase-3 after 3 h reperfusion, whereas sense-ODNs had no effect. The samples were processed using the biotin switch method followed by western blotting. n=4; *P<0.05compared with sham group, ^#P<0.05 compared with TE group. (g) TrxR2 AS-ODNs inhibited procaspase-3 activation after 6 h reperfusion, whereas sense-ODNs had no effect (n=4; *P<0.05 compared with sham group, ^#P<0.05 compared with TE group). Data are represented as means±S.D.