中文摘要：

目的通过观察脑缺血再灌注大鼠海马CAl区神经元内丝氨酸／苏氨酸蛋白激酶B（Akt）及细胞色素C的表达及定位情况，探讨延迟性脑缺血后处理神经保护作用及其可能的分子机制。方法制作SPF级成年雄性SD大鼠（40只）四动脉结扎全脑缺血模型。实验动物随机分为假手术组，缺血再灌注组，后处理组，抑制剂组及溶剂对照组。采用焦油紫染色技术观察大鼠海马CAl区神经元存活情况；Westernblotting法检测磷酸化Akt及细胞色素C的表达及定位。结果延迟性的脑缺血后处理能够促进缺血再灌注大鼠海马CAl区神经元生存；促进磷酸化Akt水平升高；阻止线粒体内细胞色素C向胞质释放；脑室注射LY294002后，细胞色素C的释放减少，抑制延迟性后处理的神经元保护作用。结论延迟性脑缺血后处理通过诱导胞质内Akt的磷酸化，抑制线粒体内细胞色素C释放到胞质，阻止全脑缺血再灌注后大鼠海马CAl区神经元损伤。

英文摘要：

Objective The goal of this study is to elucidate the neuro-protective effect and the possible mechanism of delayed ischemic postconditioning through observing the level of p-Akt and cytochrome C （ Cyt C） in cytoplasm or mitochondria following global cerebral ischemia. Methods 40 Adult male Sprague-Dawley rats were subjected to global cerebral ischemia by four-vessel occlusion and were randomly divided into five groups： sham group, ischemia.reperfusion group （I/R）, delayed ischemic postconditioning group （Post C）, Vehicle group （Post C ＋ Vehicle） and LY294002 group （Post C ＋ LY294002）. Cresyl violet staining was used to observe the surviving neurons of hippocampal CA1 region following global cerebral ischemia and western blot analysis was used to detect the level of p-Akt and Cyt C in both cytosolic and mitochondrial fraction. Results Delayed ischemic postconditioning protected the hippocampal CA1 region neurons against ischemia/referfusion injury and significantly increased the level of p-Akt in cytoplasm compared with I/R groups. Delayed ischemic postconditioning markedly prevented the release of Cyt C from mitochondria to cytoplasm and LY294002, an inhibitor of Akt up-stream kinase, abolished the positive role of delayed ischemic postconditioning. Conclusion Delayed ischemic postconditioning induces the Akt activation and prevents the release of Cyt C from mitochondria to cytoplasm, thereby blocks the hippocampal CA1 region neurons injury following global cerebral ischemia.