Skip to main content
. Author manuscript; available in PMC: 2016 Aug 3.
Published in final edited form as: FEBS J. 2015 Mar 27;282(10):2045–2059. doi: 10.1111/febs.13259

Fig. 4.

Fig. 4

PDI thiol reductase activity is inhibited in post-hypoxic neurons and post-ischemic brain. (A) The COX-2 inhibitor SC65872 attenuates decrease in PDI activity after hypoxia. Rat primary neurons were treated with dimethylsulfoxide (Veh) or SC65872 (1 μM) 2 h prior to normoxia or hypoxia. Cells were harvested 24 h later, PDI was immunoprecipitated, and PDI thiol reductase activity measured. Data are means ± SE. n = 9 per group (three independent experiments combined, n = 3 each). *P < 0.05; **P < 0.001 using one way ANOVA with Dunnett’s post hoc analysis. (B) PDI thiol reductase activity is reduced after asphyxial cardiac arrest. Male juvenile rats underwent asphyxial cardiac arrest or sham surgery (n = 8 per group) and were killed 24 h after resuscitation. Hippocampal PDI was immunoprecipitated followed by PDI thiol reductase activity assay (upper). Immunoblot of hippocampal cell lysate (lower) indicates PDI protein expression is unchanged after asphyxial cardiac arrest. Data normalized to sham and are presented as means ± SE. **P < 0.001.