基础医学与临床 ›› 2015, Vol. 35 ›› Issue (10): 1363-1368.

• 研究论文 • 上一篇    下一篇

高迁移率族蛋白B1参与心肺复苏术后大鼠海马组织p38MAPK信号通路的激活

侯安然1,康秀文2,陈晓兵2,王言理2,刘克喜1   

  1. 1. 江苏省连云港市第一人民医院
    2. 连云港第一人民医院重症监护室
  • 收稿日期:2014-12-31 修回日期:2015-05-24 出版日期:2015-10-05 发布日期:2015-09-30
  • 通讯作者: 刘克喜 E-mail:Liukexi2006@163.com

HMGB1 involved in the activation of p38MAPK signaling pathway in the hippocampus of rats after cardiopulmonary resuscitation

  • Received:2014-12-31 Revised:2015-05-24 Online:2015-10-05 Published:2015-09-30

摘要: 目的 探讨高迁移率族蛋白B1(HMGB1)在心肺复苏(CPR)术后大鼠海马组织激活p38 MAPK信号通路的作用。方法 将SD大鼠随机分为假手术组和复苏组(按复苏后自主循环恢复后2、6、12、24和48 h各时间点分5个亚组)。在相应的时间点断头处死,取海马组织,HE染色观察海马病理变化,干湿称重法测定脑组织含水量,RT-PCR法检测HMGB1mRNA表达,Western blot检测HMGB1和p38激酶活性。结果 假手术组海马组织结构未见明显变化,复苏组存在缺血病理改变,24 h最为显著。与假手术组比较:复苏组脑组织含水量、海马HMGB1mRNA表达均呈先上升后下降的趋势,于24 h达到峰值(P<0.01);复苏组HMGB1表达在ROSC后2 h显著降低,6和12 h逐渐增高,24 h达到峰值(P<0.01);复苏组海马组织p38激酶活性于2 h表达显著升高(P<0.01),6 h达到高峰(P<0.01),后缓慢下降。结论 HMGB1可能通过参与p38 MAPK信号通路的激活介导CPR术后早期脑组织炎性反应损伤。

关键词: 心肺复苏, 高迁移率组蛋白B1, p38丝裂源活化蛋白激酶, 神经炎性反应损伤

Abstract: Objective To investigate the role of HMGB1 involved in the activation of p38MAPK signal pathway in the hippocampus of rats after cardiopulmonary resuscitation. Method Rats were randomly divided into two groups as shame-operated group, CPR group including 2, 6, 12, 24 and 48 h after restoration of spontaneous circulation( ROSC) (5sub-groups).The animals were sacrificed and hippocampus were removed at the indicated time. Pathological changes were observed at each time point. Calculated the brain water content by day/wet ration.The HMGB1mRNA expression was detected by RT-PCR technique. The expressions of HMGB1 and p38MAPK activity were determined using Western blot. Results There were no histopathological in the hippocampus of rats in shame-operated group, brain tissue appeared change of ischemia pathology in CPR group, it was the most severest at ROSC 24 h. The brain water content, HMGB1mRNA in rats of CPR group increased obviously along with the prolongation of time following ROSC and reached its peak at ROSC 24 h(P<0.01),much higher than that of shame-operated group, the HMGB1 level in the hippocampus of rats after CPR significantly declined at 2 h after ROSC(P<0.01) and increased obviously at 6, 12 h and reached peak 24 h later(P<0.01), the p38MAPK activity in the hippocampus of rats after CPR, significantly increased at 2 h after ROSC and reached peak 6 h later(P<0.01), then declined slowly later, much higher than that of shame-operated group. Conclusions HMGB1 involved in the activation of p38 MAPK signal pathway that may play an important role in the early stages of brain injury after CPR.

Key words: Cardiopulmonary resuscitation, HMGB1, p38MAPK, Neuroinflammation