Abstract
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. Key words: Deep hypothermic; Cerebral protection; PDK/Akt signaling pathway
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