摘要
目的探讨p38细胞内丝裂原活化蛋白激酶通路(MAPK)通路在异氟醚诱发新生大鼠认知功能障碍中的作用。方法将60只7日龄SD大鼠随机分为5组各12只。其中A组正常饲养;B、C组均置于自制麻醉气体吸入箱中并分别吸入1.2%、1.8%异氟醚,D、E组处理分别同B、C组,但在吸入异氟醚前30 min腹腔注射p38MAPK抑制剂SB203580。6周后各组均进行行为学实验观察逃逸潜伏期(T1)、空间探索时间(T2),并取海马组织采用Western blot法测定p38蛋白含量。结果 B、C组T1均显著长于A组,而D、E组分别显著短于B、C组(P均<0.05);B、C组T2均显著短于A组,而D、E组分别显著长于B、C组;B、C组海马区p38蛋白含量显著高于A组,而D、E组分别显著低于B、C组(P均<0.05)。结论异氟醚诱发新生大鼠认知功能障碍与p38MAPK通路活化有密切关系,抑制该通路活化可减轻认知功能损害。
Objective To inve the role of p38 mitogen-activated protein kinase pathway（MAPK） in cognitive impairment for neonatal rats induced by isoflurane.Methods Sixty neonatal SD rats of 7 day-old were randomly divided into 5 groups with 12 in each.Of which group A was fed normally;group B,C inhaled 1.2% and 1.8% isoflurane respectively,group D,E were treated as group B,C,but accept intraperitoneal injection of p38MAPK inhibitor SB203580 30 min before the isoflurane inhalation.After 6 weeks,the experimental groups were observed for escape latency behavior（T1）,space exploration time（T2）by behavioral experiments（Morris water maze test）,and hippocampal tissue was taken to detect p38 protein using Western blot.Results T1 of group B,C were significantly longer than that of group A,while which of group D,E were significantly shorter than that of group B,C（all P0.05）;T2 of group B,C were significantly shorter than that of group A,while which of group D,E were significantly longer than that of group B,C（all P0.05）;the determination of p38 protein of group B,C were significantly longer than that of group A,while which of group D,E were significantly shorter than that of group B,C（all P0.05）.Conclusions Cognitive dysfunction in neonatal rats caused by isoflurane is closely related to the activation of p38MAPK pathway,to inhibit the the activation of p38MAPK pathway can lighten the cognitive dysfunction.
出处
《山东医药》
CAS
北大核心
2011年第19期21-23,共3页
Shandong Medical Journal
基金
上海市科委2009年度基础研究重点项目(09JC1405600)
