In the present study, therefore, we used a CA-induced global cerebral ischemic in vivo model to investigate whether sevoflurane post-conditioning is capable of promoting neuronal survival after global cerebral ischemia via preserving mitochondrial biogenesis and integrity and increasing expression of mitochondria-specific antioxidant enzymes, and whether this function is regulated by a mechanism involving the PI3K/Akt survival pathway. This evidence concerns the gene AKT1 and Cerebral ischemia.