摘要
目的:观察蛛网膜下腔出血后脑血管痉挛模型中海马组织内蛋白激酶B及其磷酸化的时相变化特点,初步探讨脑血管痉挛导致缺血性脑损伤时的神经保护机制。方法:实验于2004-04/08在第四军医大学基础医学部解剖学教研室实验室进行。选择健康新西兰白兔12只,随机分为两组:蛛网膜下腔出血组(n=9)和正常对照组(n=3)。建立家兔蛛网膜下腔出血后脑血管痉挛的实验模型,用Westernblot方法检测兔蛛网膜下腔出血后不同时间点海马组织内蛋白激酶B和磷酸化蛋白激酶B蛋白的表达变化。结果:12只动物均进入结果分析,Westernblot结果显示,在正常兔海马组织中检测到了蛋白激酶B,磷酸化蛋白激酶B和actin蛋白的表达,其中蛋白激酶B和actin有较高的表达水平,而磷酸化蛋白激酶B仅微弱表达。蛋白激酶B在蛛网膜下腔出血组各时间点的海马组织内的表达保持相对恒定。磷酸化蛋白激酶B的表达水平在蛛网膜下腔出血组1d时即明显升高(P<0.05),4d时达高峰,7d时仍维持较高水平,与正常组比差异显著(P<0.01),分别是其在正常组海马中表达水平的2.1,4.4和3.1倍。结论:蛋白激酶B信号通路的激活与海马缺血损伤的程度在时程上有伴行关系,从而发挥了对蛛网膜下腔出血后脑血管痉挛所造成的海马神经元损伤的神经保护作用。
AIM:To observe the temporal changes and phosphorylation status of Akt in hippocampus after cerebral vasospasm(CVS) following subarachnoid hemorrhage(SAH),and primarily investigate the neuroprotective mechanisms during ischemic brain injury induced by CVS. METHODS:The experiment was performed in the Department of Anatomy,Institute of Basic Medicine,Fourth Military Medical University of Chinese PLA,from April to August 2004.Twenty New Zealand rabbits were divided into two groups:SAH group(n=9) and control group(n=3).The model of CVS following SAH was established. Western blot was used to detect the changes of the expression of AKt and phosphorylated Akt(p Akt) protein in rabbit hippocampus at different time points following experimental SAH. RESULTS:All 12 rabbits were analyzed.Western blot indicated that the expression of Akt,p Akt and β actin protein was detected in normal rabbit hippocampus.The Akt and β actin protein expressed significantly;however,p Akt expressed weakly.The expression level of Akt protein in hippocampus kept unchanged in SAH group.However,the expression of p Akt protein significantly increased in hippocampus at 1 day after SAH(P< 0.05),reached to the peak at 4 day and kept a higher level at 7 day,and there was significant difference as compared with those in the control group(P< 0.01),which was 2.1,4.4 and 3.1 times higher than that in the control group, respectively. CONCLUSION:The present results suggest that the activation of Akt signal pathway has the concomitant relation with the degree of ischemic brain injury in hippocampus in a timely manner,so as to play important neuroprotective roles during the CVS induced hippocampus injury following SAH.
出处
《中国临床康复》
CSCD
北大核心
2005年第13期86-87,共2页
Chinese Journal of Clinical Rehabilitation
