内毒素诱导幼年大鼠脑神经细胞凋亡及脑组织ERK表达的变化  

The apoptosis of neuron and expression of ERK in cortex induced by endotoxemia in young rats

作　　者：李哲[1] 赵亚娟[2] 

机构地区：[1]沈阳市儿童医院急诊科,110031 [2]中国医科大学附属盛京医院儿科,沈阳110004

出　　处：《中国小儿急救医学》2010年第5期437-438,共2页Chinese Pediatric Emergency Medicine

摘　　要：目的研究ERK在内毒素诱导脑神经细胞凋亡中的作用，为早期干预提供理论依据。方法10Et龄Wistar大鼠，随机分为LPS诱导脑损伤组（LPS组）和生理盐水组（NS组）。于腹腔注射后6、12、72h采用原位细胞凋亡检测法（TUNEL法）检测脑组织细胞凋亡情况，采用免疫组织化学法检测脑组织ERK表达情况，阳性细胞的染色强度转变为量化指标，计算其平均光密度。结果（1）LPS组6h开始出现凋亡细胞，但凋亡指数与NS组差异元显著性（P〉0．05），12h可见凋亡细胞数逐渐增多，72h最多，明显高于NS组，差异有显著性（P〈0．05，P〈0．01）。（2）6h时LPS组ERK表达高于NS组，差异有非常显著性（P〈0．01）。12h时LPS组ERK表达下降，低于NS组，差异有非常显著性（P〈0．01）。72h时两组间差异无显著性（P〈0．05）。结论内毒素可以诱导幼年大鼠脑神经细胞凋亡，ERK被激活可能参与凋亡的发生。Objective To investigate the effect of ERK in apoptosis of neuron induced by endotox- emia,provide the theory basis for the early intervention. Methods Wistar rats aged 10 day were randomly divided into two groups：LPS group and NS group. Neuron apoptosis at 6、12,72 h after abdomen injection were detected by TUNEL method, the expressions of ERK were measured by immunohistoehemial method. Results （ 1 ） apoptosis cell appeared at 6 hour in LPS group, but the apoptosis index showed no difference from NS group（P 〉0. 05）. The apoptosis cell obvious increased at 12 hour,peaked at72 hour（P 〈0. 05 ,P 〈 0. 01 ）. （2）As compared with NS group, the expression of ERK increased at 6 h（ P 〈 0. 01 ）, obviously decreased at 12 h （ P 〈 0. 01 ）, and reversed to the level of NS group at 72 h （ P 〉 0. 05 ）. Conclusion LPS can induce the neuron apoptosis in young rats, the ERK is activated and could play role in apoptosis.

关 键 词：内毒素 脓毒症 细胞凋亡 大鼠 

分 类 号：R285.5[医药卫生—中药学]