CAJ | 학술논문

目的:研究缺血缺氧新生大鼠海马结构(主要为 CA1)磷酸化 c-AMP反应元件结合蛋白质( phosphorylated cylic AMP response element binding protein,p-CREB)变化以及 GM1对其的影响. 方法 :7 d龄 SD仔鼠共 108只,随机分为 3组:假手术对照组( 36只),缺血缺氧组( HI组 ,36只)及缺血缺氧+神经节苷脂组( GM1组, 36只),于模型建立后 1, 4, 12, 24, 48和 72 h处死,免疫组化观察海马 CA1区 p-CREB的变化. 结果 :对照组各时间点之间 p-CREB的表达差异无显著性意义( F=0.48,P >0.05); HI组、 GM1组 CA1区 p-CREB的表达一过性升高后迅速下降 ,HI组、 GM1组与对照组相比有明显的差异 (P< 0.05);HI组与 GM1相比无明显差异 (P >0.05). 结论 :缺血缺氧后缺血敏感 CA1区 p-CREB的表达呈现一过性的升高后迅速下降, GM1不能抑制 p-CREB的表达 ,对神经元的存活没有损害作用 ,具有较大的临床应用潜能.
목적:연구결혈결양신생대서해마결구(주요위 CA1)린산화 c-AMP반응원건결합단백질( phosphorylated cylic AMP response element binding protein,p-CREB)변화이급 GM1대기적영향. 방법 :7 d령 SD자서공 108지,수궤분위 3조:가수술대조조( 36지),결혈결양조( HI조 ,36지)급결혈결양+신경절감지조( GM1조, 36지),우모형건립후 1, 4, 12, 24, 48화 72 h처사,면역조화관찰해마 CA1구 p-CREB적변화. 결과 :대조조각시간점지간 p-CREB적표체차이무현저성의의( F=0.48,P >0.05); HI조、 GM1조 CA1구 p-CREB적표체일과성승고후신속하강 ,HI조、 GM1조여대조조상비유명현적차이 (P< 0.05);HI조여 GM1상비무명현차이 (P >0.05). 결론 :결혈결양후결혈민감 CA1구 p-CREB적표체정현일과성적승고후신속하강, GM1불능억제 p-CREB적표체 ,대신경원적존활몰유손해작용 ,구유교대적림상응용잠능.
AIM:To study the expression of phosphorylated regulatory element-binding protein(p-CREB) in hippocampus(CA1) of neonatal cerebral hypoxia-ischemia(HI,n=36) rat and the effect of gangliosides (GM1). METHODS:108 pieces of SD rats were randomly divided into three groups:control group(n=36),hypoxic-ischemia group(HI,n=36),and hypoxic-ischemia with GM1 group(GM1,n=36).The level of the p-CREB in hippocampus(CA1) were observed respectively at 1,4,12,24,48 and 72 hours after hypoxic-ischemia managements. RESULTS:The p-CREB levels in CA1 of control group had no difference at different times(P >0.05);the p-CREB level in CA1 f HI and GM1 group decreased quickly after a transient increase;there were significant differences between HI group and control group as well as between GM1 group and control group(P< 0.05);there was no significant difference between HI group and GM1 group(P >0.05). CONCLUSION:p-CREB level in CA1 of HI group decrease quickly after a transient increase compared with control group after HI management;the expression of p-CREB in CA1 is not suppressed by GM1,which is no harm to neurone survival,and therefore with potential clinical applications.