Correlative Study on Calcium Influx and Expression of p53 Gene and Apoptosisin in Cerebral Cortical Cells of Neonatal Pigs Following Hypoxic Ischemic Encephalopathy.

Objective To determine whether there is apoptosis in cerebral cortical of the neonates following hypoxic ischemic encephalopathy(HIE)and the correlative inducement. Method 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 Hl.The CAR 72hr later post Hl in experimental group was significantly higher than those in control group and in Nimotop group( n =15,12,13; ±s =27.50±16.20,3.23±2.93,9.17±5.76; F =18.756 4, P 0.000 1);IFCa level and the positive expression of p53 protien 4hr later post HI in experimental group increased obviously( n =12,12,12; ±s =348.96±39.59,160.98±37.05,260.81±66.81, F =41.168 1, P 0.000 1; ±s =6.07±5.55, 1.18±0.53, 3.13±2.18, F =6.0767, P =0.0057).An obvious correlation existed between IFCa level and expression of p53 gene 4hr later post Hl( r =0.497 7, P =0.002).A positive correlation between CAR 72hr later and IFCa level 4hr later post HI ( r =0.661 5, P 0.001)was found.The'DNA Ladder'was correponded to appearance of the apoptosis peak observed by FCM. Conclusion The apoptosis of cerbral cortical cells plays an important role in the delayed cerebral damage of the neonates following Hl,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.