RESUMEN
AIM: To investigate the PI3K/AKT/GSK-3β signaling pathway involved in the protective effect and mechanism of propofol on the cerebral ischemia-reperfusion injury in rats. METHODS: There were 72 healthy male SD rats. All rats established a model of focal cerebral ischemia-reperfusion injury according to the Zea Longa method and were randomly divided into six groups (n=12), A-sham operation group, B-model group (MCAO), C-Propofol group, D-Propofol+adenosine A1R antagonist group (DPCPX), E-Propofol group+PI3K specific inhibitor (LY294002), F-Propofol+GSK3β inhibitor group (SB216763). The neurological scores of rats 24 h after operation, LDF monitors changes in cerebral blood flow before and after embolization were observed. The TTC staining method was used to detect the cerebral infarction volume of rats in each group; HE staining method was used to observe the morphological changes of the rat brain tissue; Immunohistochemical method was used to detect Bcl-2 positive cells expression; TUNEL was used to detect cerebral cortex ischemia in each group. The percentage of neuronal apoptotic cells. RESULTS: Compared with group A, the behaviors, cerebral infarction volume, apoptosis rate, and Bcl-2 protein expression of rats in groups B, C, D, E, and F all increased (P<0.05); compared with group C, the behavioral scores, cerebral infarction volume and apoptosis rate of rats in groups B, D and E all increased significantly, and the expression of Bcl-2 protein was decreased significantly (P<0.01), but the expression of Bcl-2 protein in group F was increased, cell apoptosis rate decreased (P<0.05), behavior score and infarcts decreased (P<0.05). CONCLUSION: The neuroprotective effect of propofol mediated by adenosine A1R on ischemia-reperfusion injury in rats may be related to the PI3K/AKT/GSK-3β signal transduction pathway.