CORRELATIVE STUDY ON CALCIUM
INFLUX AND EXPRESSION OF P53 GENE AND APOPTOSIS IN CEREBRAL CORTICAL CELLS
OF NEONATAL PIGS FOLLOWING HYPOXIC-ISCHEMIC-ENCEPHALOPATHY
Wang Xiaolei, Liu X-P, Liu K, et al.
Department of Pediatrics
& Biomedical Laboratory, Third Municipal Hospital of Chengdu, Sichuan,
China
Objective: To determine whether there is apoptosis in cerebral
cortical cells of the neonates following hypoxic-ischemic-encephalopathy
(HIE) and the correlative inducement.
Methods: The ¡®DNA Ladder¡¯ was observed by gel electrophoresis
and the dynamic changes of cerebral apoptosis ratio(CAR) and the
intracellular free Calcium (IFCa) level and the expression of p53 gene were
investigated via Flow Cytometry (FCM).
Results: We found that there was no obvious apoptosis in
ipsilateral frontotemporal corticocerebrum 4hr later post HI. The CAR 72hr
later post HI in experimental group was significantly higher than those in
control group and in Nimotop group (n=15, 12, 13; x¡Às=27.50¡À16.20,
3.23¡À2.93,
9.17¡À5.76;
F=18.7564, P<0.0001); IFCa level and the positive expression of p53
protein 4hr later post HI in experimental group increased obviously (n=12,
12, 12; x¡Às=348.96¡À39.59,
160.98¡À37.05,
260.81¡À66.81,
F=41.1681, P<0.0001, x¡Às=6.07¡À5.55, 1.18¡À0.53,
3.13¡À2.18,
F=6.0767, P=0.0057). An obvious correlation existed between IFCa level and
expression of p53 gene 4hr later post HI(r=0.4977, P=0.002). A positive
correlation between CAR 72hr later and IFCa level 4hr later post HI
(r=0.6615, P<0.001) was found. The ¡®DNA Ladder¡¯ was corresponded to
appearance of the apoptosis peak observed by FCM.
Conclusion: It suggested that the apoptosis of cerebral
cortical cells plays an important role in the delayed cerebral damage of
the neonates following HI, and that this apoptosis can be induced mainly by
means of activation of Calcium channel and proper usage of Calcium channel
blockers-Nimotop can partially inhibit this apoptosis. Simultaneously, the
damage of cellular DNA following HIE is also an important inducement of the
apoptosis.