A
MOLECULAR BIOLOGICAL STUDY ON THE RESISTANCE TO BRAIN DAMAGE INDUCED BY
PROLONGED SEIZURE IN PREMATURE BRAIN
JIANG L, CAI FC, ZHANG XP
Children’s Hospital, Chongqing University of
Medical Sciences, Chongqing, China
Objective: On the base of our former
research, to explore the molecular biological base of internal protective
response in premature brain which reducing the process of apoptosis and
necrosis of neurons after prolonged seizure.
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, 2, 8, 24, 48, and 72 hours after prolonged seizure stopped.
Hippocampus, dentate gyrus and parietal cortex of their brain were taken
for immunocytochemistry and Western blot studies for apoptosis associated
genes bcl-2 and P53 expression.
Results: (1) In ARs group, 90% of
the animal’s brain with positive P53 expression, and 56% of them was in
meddle and strong expression ,and such state continually keep even at 72h
after seizure; however bcl-2 expression was low and weak ( positive bcl-2
expression was 57%, and 73% of them only with weak expression), and no
difference was found on bcl-2 expression only in several hours comparing
with normal control. (2) In BRs’ brain, there was more than 85% animal
brain with a strongest expression of bcl-2; and the strongest bcl-2
expression sustained in 72h after SE, however P53 expression was only 65%,
and most of them (61%) with weak expression and P53 expression only lasted
less than 24h.
Conclusion: Significant difference between premature and mature
brain was shown on the genes’ expression associated apoptosis after
seizure. Anti apoptosis gene (bcl-2) expression was much higher and longer
than apoptosis gene (P53) in BRs’ brain, and it was reversed in Ars group.
So stimulating bcl-2 expression and inhabiting of P53 expression after SE
could be the important molecular biological basis for the special
resistance to neuron injury in premature brain.