CAJ | 학술논문

目的探讨蛋白激酶C(PKC)在新生儿缺氧缺血性脑病(HIE)发病机制中的作用.方法 24只大鼠随机分为3组:正常对照组(N),模型对照组(C).HIE组(HIE);利用SDS-聚丙烯酰胺凝胶电泳(SDS-PAGE)、蛋白印迹(Western-blot)等生化技术,观察脑皮层和海马PKC膜转位的变化.结果 N组皮层、海马PKC膜转位水平分别为0.28±0.02、0.29±0.02;C组为0.29±0.02、0.30±0.02;HIE组为0.38±0.04、0.40±0.06;HIE组皮层、海马PKC膜转位水平明显增高,分别与N组、C组相比,有明显差异(P＜0.01),N组和C组相比,差异无显著性(P＞0.05).结论 PKC可能参与HIE病理生理机制的形成.
목적 탐토단백격매C(PKC)재신생인결양결혈성뇌병(HIE)발병궤제중적작용.방법 24지대서수궤분위3조:정상대조조(N),모형대조조(C).HIE조(HIE);이용SDS-취병희선알응효전영(SDS-PAGE)、단백인적(Western-blot)등생화기술,관찰뇌피층화해마PKC막전위적변화.결과 N조피층、해마PKC막전위수평분별위0.28±0.02、0.29±0.02;C조위0.29±0.02、0.30±0.02;HIE조위0.38±0.04、0.40±0.06;HIE조피층、해마PKC막전위수평명현증고,분별여N조、C조상비,유명현차이(P＜0.01),N조화C조상비,차이무현저성(P＞0.05).결론 PKC가능삼여HIE병리생리궤제적형성.
Objective To explore the role of protein kinase(PKC)in the nosogenesis of hypoxic-ischemic encephalopathy(HIE).Methods Twenty-four seven-day-old SD rats were divided randomly into normal group (N),model control group(C)and HIE group(HIE).The biochemistry techniques of SDS-PAGE and western bolt were used to examine the level of PKC membrane translocation of cortex and hippocampi.Results The level of PKC membrane translocation of cortex and hippocampi in N group was 0.28±0.02,0.29±0.02 respectively,and 0.29±0.02,0.30±0.02 in C group,and 0.38±0.04,0.40±0.06 in group HIE.The level of PKC membrane translocation of cortex and hippocampi was higher in HIE group as compared with that in N,C group(P＜0.01),but there was no different between N group and C group(P＞0.05).Conclusion PKC are activated in HIE,which indicates that PKC may involve in the pathophysiologic mechanism of HIE.