中文摘要：

目的 观察PI3K/Akt在深低温低流量（DHLF）脑保护中的作用并探讨其机制.方法 Akt1＋/-小鼠与野生型（WT）小鼠各48只分别随机并平均的分为假手术组与手术组.手术组在深低温下钳闭颈总动脉120 min并重新开放,模拟DHLF过程.各组脑血流经激光多普勒血流仪监测.经TUNEL和Western blot检测各组脑细胞凋亡及Akt下游bcl-2与bax的改变.结果 阻断颈总动脉后,小鼠脑血流量减少86%以上.野生型手术组死亡率在再灌注24h后约为15%,72h死亡率达到20%,而Akt1＋/-小鼠死亡率增加,24h后约为25%,72 h达到40%（P〈0.05）.Akt1＋/-脑细胞凋亡数量增多（P〈0.01）,Western blot显示Akt下游bcl-2与bax表达增强.结论 抑制Akt1后小鼠脑损害程度加重,PI3K/Akt通过抑制线粒体凋亡通路发挥作用.

英文摘要：

Objective To investigate the genetic effect of PI3K/Akt signaling pathway in Akt1＋/-mice after deep hypothermia low flow （ DHLF）. Methods Ninety-six Akt1＋/- and wild-type C57/B6 mice were randomly and equally divided into sham-operation and operation groups. The Akt1＋/- and wild type of C57BL/6 mice underwent bilateral common carotid arteries occlusion for 120 min at （18.5 ± 0. 5）℃. and then reopened and rewarmed, while the sham-operation group excluded the occlusion. Regional cerebral blood flow （rCBF） was determined by laser Doppler flowmetry （LDF）. By using TUNEL and Western blotting, the apoptotic level of cerebral cells and expression of bcl-2 and bax were examined. Results rCBF was decreased by at least 86% after occlusion. Mortality of Akt1＋/- mice was increased to 25% after 24 h of cerebral reperfusion and 40% after 72 h （P 〈0. 05）. Western blotting showed the expression of bcl-2 and bax at the downstream of Akt1 was increased. Conclusion Haplo-insufficiency of Akt1 exacerbates cerebral injury after DHLF. PDK/Akt exerts their roles by inhibiting the apoptosis pathway in mitochondria.