›› 2011, Vol. 42 ›› Issue (2): 164-169.doi: 10.3969/j.issn.0529-1356.2011.02.005

• 论著 • 上一篇    下一篇

p-Akt、Bid与小鼠局灶性脑缺血后处理保护作用的关系

刘媛媛1;崔颖2;高俊玲1* ;田艳霞1;冉芳1;李冉1;崔建忠3   

  1. 1. 华北煤炭医学院基础医学部, 河北 唐山063000;2河北医科大学临床医学系, 石家庄050017;3. 唐山市工人医院神经外科, 河北 唐山063000
  • 收稿日期:2010-02-22 修回日期:2010-04-16 出版日期:2011-04-06
  • 通讯作者: 高俊玲

Relationship between Akt signal pathway and the protective effects of focal cerebral ischemic postconditioning in mice

  1. 1. Department of Basic Medicine, North China Coal Medical College,Hebei,Tangshan063000,China;2. Department of Clinical Medicine, Hebei Medical University, Shijiazhuang050017,China;3Department of Nurosurgery, Tanshan Worker’s Hospital, Hebei Tangshan063000, China
  • Received:2010-02-22 Revised:2010-04-16 Online:2011-04-06
  • Contact: GAO Jun-ling

关键词: 缺血再灌注损伤, 缺血后处理, p-Akt, Bid, 免疫组织化学, 免疫印迹法, 氯化三苯基四氮唑染色, 小鼠

Abstract: P>ObjectiveTo investigate the changes in p-Akt and Bid after ischemia reperfusion(I/R)injury and ischemic postconditioning(IP),and the relationship between p-Akt and IP. MethodsFocal ischemia was generated by transient middle cerebral artery occlusion(MCAO). Totally 315 male Kunming mice were randomly divided into four groups:Sham group,I/R group,IP group,IP plus LY group.At the right time point,the brain tissue samples were prepaired for brain histology and determination of the experssion of p-Akt and Bid,by means of immunohistochemistry and Western blotting.The volume ratio of the cerebral infarction was estimated by 20 g/L TTC staining. ResultsIn the cytoplasm of nerve cells,the levels of Akt and Bid were higher in I/R mice than those in Sham mice.The expression of p-Akt in the cytoplasm began to increase at the 0.5 hour, increased to the highest level at the 1st hour (EM>P/EM><0.05),and then gradually returned to the basic level.But the expression of Bid began to increase at the 6th hour, increased to the highest level at the 24th hour(EM>P/EM><0.05),and then returned gradually; At the corresponding time,compared with I/R group,the expression of p-Akt increased remarkably in IP group(EM>P/EM><0.05); meanwhile, the expression of Bid decreased significantly in IP group (P<0.05).LY294002,a specific blocker of PI-3K,notably blocked PI-3K/Akt signal pathway and inhibited the protective effects of IP in the brain. The experssion of p-Akt negatively correlated with the activated Bid (EM>r/EM> =-0.826 5, EM>P/EM><0.05).ConclusionThe protective effects of IP in the mice brain is exerted through regulating Akt signal pathway.Perhaps,the up\|regulation of the activation of P1-3K/Akt system is one of the mechanism through which the protective effects of IP can exert .Bid is involved in the process of IP. Akt can regulate the expression of Bid through the death receptor signal pathway./P>

Key words: Ischemia reperfusion injury, Ischemic postconditioning, p-Akt, Bid, Immunohistochemistry, Western blotting, TTC staining, Mouse

中图分类号: