Ischemic preconditioning (IPC) is a condition of sublethal transient global
ischemia and exhibits
neuroprotective effects against subsequent lethal ischemic insult. We, in this study, examined the
neuroprotective effects of IPC and its effects on immunoreactive changes of
antioxidant enzymes including
superoxide dismutase (SOD) 1 and SOD2,
catalase (CAT) and
glutathione peroxidase (GPX) in the gerbil hippocampal CA1 region after transient forebrain
ischemia. Pyramidal neurons of the stratum pyramidale (SP) in the hippocampal CA1 region of animals died 5 days after lethal transient
ischemia without IPC (8.6% (ratio of remanent neurons) of the
sham-operated group); however, IPC prevented the pyramidal neurons from subsequent lethal ischemic injury (92.3% (ratio of remanent neurons) of the
sham-operated group). SOD1, SOD2, CAT and GPX immunoreactivities in the
sham-operated animals were easily detected in pyramidal neurons in the stratum pyramidale (SP) of the hippocampal CA1 region, while all of these immunoreactivities were rarely detected in the stratum pyramidale at 5 days after lethal transient
ischemia without IPC. Meanwhile, their immunoreactivities in the
sham-operated animals with IPC were similar to (SOD1, SOD2 and CAT) or higher (GPX) than those in the
sham-operated animals without IPC. Furthermore, their immunoreactivities in the stratum pyramidale of the
ischemia-operated animals with IPC were steadily maintained after lethal
ischemia/reperfusion. Results of western blot analysis for SOD1, SOD2, CAT and GPX were similar to immunohistochemical data. In conclusion, IPC maintained or increased the expression of
antioxidant enzymes in the stratum pyramidale of the hippocampal CA1 region after subsequent lethal transient forebrain
ischemia and IPC exhibited
neuroprotective effects in the hippocampal CA1 region against transient forebrain
ischemia.