[Objective] To explore the effects and possible roles of treatment with ischemia postconditioning (IPC) on the cognitive impairment and alterations of mTOR/AKT proteins in ischemia/reperfusion (I/R) injured rat model.[Methods] The thirty female Sprague-Dawley (SD) rats were divided into three groups:sham operated group, I/R group and IPC treated group. There were ten rats in each group. The neurological score and Morris Water Maze (MWM) test were used to evaluate the functional impairment after injury. At the end of the MWM test, the rats were sacrificed and the hippocampus was harvested for detection of Synaptophysin, mTOR, p-mTOR, AKT and p-AKT expressions. Immunohistochemistry staining was employed to detect the distribution and expressions of NeuN, GFAP and mTOR in the hippocampus of rats. Western blot were employed and Synaptophysin levels, the ratio of p-mTOR/total-mTOR, as well as p-AKT/total-AKT were calculated.[Results] Compared with that of I/R group, rats in IPC group showed significant cognitive improvement, in which the rats revealed shorter escape latency and more duration in the target quadrant (P<0.05). After IPC treatment, AAR was shorten than that of I/R group(P<0.05). Meanwhile, the IPC increased the NeuN immuno-positive files and Synaptophysin protein level, decreased the GFAP immunohistochemistry positive cells, significantly enhanced the phosphorylation of mTOR and AKT (P<0.05).[Conclusion]1. Cognitive improvement induced by IPC in I/R rats is associated with NeuN positive neurons compensation, decreased the reactive hyperplasia of astrocyte induced by I/R, as well as the actived mTOR/AKT signaling pathway;2. It is a promised therapeutic strategy to intervene the mTOR/AKT signaling pathway following I/R. |