p63 is a
transcription factor of p53 gene family, which are involved in development, differentiation and cell response to stress; however, its roles in ischemic preconditioning (IPC) in the brain are not clear. In the present study, we investigated the effect of IPC on p63 immunoreactivity caused by 5 min of
transient cerebral ischemia in gerbils. IPC was induced by subjecting the gerbils to 2 min of transie
ischemia 1 day prior to 5 min of transient
ischemia. The animals were randomly assigned to four groups (
sham-operated-group,
ischemia-operated-group, IPC plus (+)-
sham-operated-group and IPC +
ischemia-operated-group). The number of viable neurons in the stratum pyramidale of the hippocampal CA1 region (CA1) was significantly increased by IPC +
ischemia-operated-group compared with that in the
ischemia-operated-group 5 days after ischemic insult. We found that strong p63 immunoreactivity was detected in the CA1 pyramidal neurons in the
sham-operated-group, and the immunoreactivity was decreased with time after
ischemia-reperfusion. In addition, strong p63 immunoreactivity was newly expressed in microglial cells of the CA1 region from 2 days after
ischemia-reperfusion. In all the IPC +
sham-operated-groups, p63 immunoreactivity in the CA1 pyramidal neurons was similar to that in the
sham-operated-group, and the immunoreactivity was well maintained in the IPC +
ischemia-operated-groups after
cerebral ischemia. In brief, our present findings show that IPC dramatically protected the reduction of p63 immunoreactivity in the pyramidal neurons of the CA1 region after
ischemia-reperfusion, and this result suggests that the expression of p63 may be necessary for neurons to survive after
transient cerebral ischemia.