The activation of the [Ca(2+)]-dependent
cysteine protease calpain plays an important role in ischemic injury. Here, the levels of two
calpain-specific substrates, p35
protein and
eukaryotic initiation factor 4G (
eIF4G), as well as its physiological regulator
calpastatin, were investigated in a rat model of transient global
cerebral ischemia with or without ischemic tolerance (IT). Extracts of the cerebral cortex, whole hippocampus and hippocampal subregions after 30 min of
ischemia and different reperfusion times (30 min and 4 h) were used. In rats without IT, the p35 levels slightly decreased after
ischemia or reperfusion, whereas the levels of p25 (the truncated form of p35) were much higher than those in
sham control rats after
ischemia and remained elevated during reperfusion. The
eIF4G levels deeply diminished after reperfusion and the decrease was significantly greater in CA1 and the rest of the hippocampus than in the cortex. By contrast, the
calpastatin levels did not significantly decrease during
ischemia or early reperfusion, but were upregulated after 4 h of reperfusion in the cortex. Although IT did not promote significant changes in p35 and p25 levels, it induced a slight increase in
calpastatin and
eIF4G levels in the hippocampal subregions after 4 h of reperfusion.