Objective:To explore the molecular biological base of internal protective response in premature brain which reduces the process of apoptosis and necrosis of neurons.Methods:Megimide was injected in healthy adult and baby rats(ARs & BRs) respectively to evoke prolonged seizures and status epilepticus(SE).ARs and BRs rats were sacrificed at 1

2

4

12

24

48

72 hours and 7 days after prolonged seizure stopped.Hippocampus

dentate gyrus and parietal cortex of their brain were taken for immunocytochemistry studies for apoptosis associated genes bcl-2 and P53 expression.Results:(1) There was a much stronger and higher rate(90%) of P53 expression in ARs’ brain

and such state continually kept even at 72h after seizure stopped;however bcl-2 expression was weak and low(57%)

and no difference was found in bcl-2 expression only several hours compared with normal control.(2) In BRs’ brain there was more than 85% neurons within a strongest expression of bcl-2;and the strongest bcl-2 expression sustained in 72h after SE

however P53 expression lasted less than 24h.Conclusion:Significant difference between premature and mature brain is shown on the genes’ expression associated apoptosis after seizure.Anti apoptosis gene(bcl-2) expression is much higher and longer than apoptosis gene(P53) in BRs’ brain

and it is reversed in ARs group.So the strongest expression of bcl-2 after SE could be the important molecular biological basis for the special resistance to neuron injury in premature brain.