脑缺血损伤与Akt研究的进展

Cerebral ischemic injury and Akt

目的:了解脑缺血过程中Akt的抗损伤作用。资料来源:应用计算机检索PubMed数据库1999-01/2005-01与Akt,脑缺血相关文章,检索词“Akt,ischemic,brain”,限定为English。资料选择:纳入标准:①随机对照实验。②Akt生物学特性研究。③脑缺血损伤研究。排除标准:综述类文献。对检索出的文献查找全文,筛除不相关的文献和重复的文献,保留近期和发表在权威杂志的文献。资料提炼:共收集到18篇,其中8篇关于Akt生物学特性、5篇脑缺血损伤、余下5篇与两者均有关系。资料综合:Akt是磷脂酰肌醇-3羟基激酶下游关键效应分子,激活后可通过灭活凋亡效应分子如叉头转录因子、半胱氨酸天冬氨酸蛋白酶9、糖原合成酶激酶3和BAD等而促进细胞存活。增加其活性具有抗缺血损伤作用。脑缺血可导致能量缺乏、Akt活性变化和细胞死亡。结论:增加Akt的生物学活性特征决定其活性可提高脑组织抗缺血损伤的能力。

OBJECTIVE:To study the roles of Akt against cerebral ischemic injury during cerebral ischemia.DATA SOURCES:Using the key terms “Akt,ischemic,brain',we searched the PubMed database for the relevant articles about Akt and cerebral ischemia published from January 1999 to January 2005 in English.STUDY SELECTION:The inclusive criteria were ①randomized controlled trials;②researches on Aktbiological characteristics;③researches on cerebral ischemic injury.Summarizations were excluded.The full text was looked up,and the noncorrelative and duplicated articles were excluded.Articles published on authoritative magazines or recently were selected.DATA EXTRACTION:A total of 18 articles were collected,8 of which were about Aktbiological characteristics,5 about cerebral ischemic injury,and 5 about both Akt and cerebral ischemic injury.DATA SYNTHESIS:Akt was a key effector downstream of phosphatidylinositol 3kinase.Activation of Akt could promote cell survival through inactivating proapoptotic molecules such as forkhead transcription factor,caspase9,glycogen synthetase3,and BAD.Increasing the activity of Akt was benefit to protection of cerebral ischemic injury.Ischemia could cause lacking energy,changes of Akt activity,and apoptosis of neurons.CONCLUSION:Increased Aktbiological characteristics makes it sure that the activity of Akt can increase the ability in protecting cerebral ischemic injury.