This study aims to establish
pilocarpine-induced rat model of
status epilepticus (SE), observe the activity of
calpain I in the rat hippocampus and the subsequent neuronal death, and explore the relationship between
calpain I activity and neuronal death in the hippocampus. Fifty-eight adult male Wistar rats were assigned randomly into either control group (n = 8) or
epilepsy group (n = 50). SE was induced in the
epilepsy group using
pilocarpine. Before the injection, the rats were given
atropine sulfate to reduce the side effect of
pilocarpine. All rats in the seizure group were grouped into either SE or non-SE, depending on whether they developed convulsive
seizures. The rats in SE group were treated with
chloral hydrate to stop
seizures after 60 min. Control animals were treated with the same dose of
0.9 % saline. All rats were monitored for
seizures. At 24 h after SE, the rats' left brain tissues were stained by HE and TUNEL. Neuronal
necrosis and apoptosis in the hippocampal CA3 area were observed.
Calpain I activity in the right hippocampus was also observed using western blotting. Eighty percent of the rats in the seizure group developed SE, of which 35 % died. No rat died in both the control and non-SE groups. At 24 h after SE, the number of HE-stained neurons decreased (SE group: 55.19 ± 8.23; control group: 102.13 ± 3.73; non-SE group: 101.2 ± 2.86) and the number of TUNEL-positive neurons increased (SE group: 4.91 ± 1.35; non-SE and control group: 0). No obvious changes were observed in the neurons of the control and non-SE group animals. The 76 kDa cleavage of
calpain I (the average optical density ratio is 0.096 ± 0.015) emerged in the SE group. Neuronal death has a direct relationship with
calpain I activity. There is high success rate and lower death rate for
pilocarpine to induce SE. At 24 h after SE, activity of
calpain I, neuronal
necrosis and apoptosis increased in the hippocampus. Neuronal death has a direct relationship with
calpain I activity, which suggests that
calpain I plays an important role in neuronal damage during SE.