Abstract:

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.

Key words: Global cerebral ischemia , Delayed ischemic postconditioning , Akt, Cytochrome C , Western blotting , Rat