The
thioredoxin (Trx) and
peroxiredoxin (Prx) redox system is associated with neuronal damage and
neuroprotective effects via the regulation of oxidative stress in
brain ischemia. In the present study,
ischemia-induced changes in the
protein expression levels of Trx2 and Prx3 in the stratum pyramidale (SP) of the hippocampal CA1 region were investigated in adult and aged gerbils, subjected to 5 min of transient global
cerebral ischemia, using immunohistochemistry and western blot analysis. In the adult
ischemia-group, minimal Trx2 immunoreactivity was detected in the SP 2 days after
ischemia-reperfusion. In the aged animals, the Trx2 immunoreactivity in the
sham-group was marginally lower compared with that in the adult
sham-group. In the aged
ischemia-group, Trx2 immunoreactivity in the SP was significantly higher 1, 2 and 4 days post-
ischemia, compared with that in the adult
ischemia-group and, in the 5 days post-
ischemia group, Trx2 immunoreactivity was significantly decreased in the SP. Prx3 immunoreactivity in the SP of the adult
ischemia-group was significantly decreased from 4 days after
ischemia-reperfusion. In the aged animals, Prx3 immunoreactivity in the
sham-group was also marginally lower compared with that in the adult
sham-group. Prx3 immunoreactivity in the aged
ischemia-group was also significantly higher 1, 2 and 4 days post-
ischemia, compared with the adult
ischemia-group; however, the Prx3 immunoreactivity was significantly decreased 5 days post-
ischemia. The western blot analyses revealed that the pattern of changes in the
protein levels of Trx2 and Prx3 in the adult and aged hippocampal CA1 region following ischemic damage were similar to the results obtained in the immunohistochemical data. These findings indicated that
cerebral ischemia lead to different
protein expression levels of Trx2 and Prx3 in the hippocampal CA1 region between adult and aged gerbils, and these differences may be associated with more delayed neuronal death in the aged gerbil hippocampus following transient global
cerebral ischemia.