The protection of inhalation anesthesia isoflurane against cerebral ischemia-reperfusion injury in rats

Objective To investigate the mechanism of isoflurane preconditioning' s neuroprotection against global cerebral ischemia in rat. Methods Global cerebral ischemia was induced by occlusions of bilateral common carotid and vertebral arteries (four vessels). Male healthy S-D rats (weighing 250 g-300 g) were selected according to model criteria and randomly divided into four groups: sham operation group (S), ischemia group ( I/R), 2 h O2 preconditioning ischemia group ( I/R +O2), and 2 h 1.5 MACisoflurane preconditioning ischemia group ( I/R + ISO) . After 15 rain global cerebral ischemia, each group was divided into two subgroups according to reperfusion time : 3 d, 5 d. The hippocampus of reperfusion 3d' s rat were undertaked to western blotting and immunoprecipitation ; the hippocampus of reperfusion 5d's rat were stained with Cresyl violet and examined the hippocampal CA1 pyramidal cells. Results After repeffusion 3 d, 2 h 1.5 MAC isoflurane preconditioning obviously inhibits the activity of JNK3 induced by focal cerebral ischemia(P <0.05 ). After reperfusion 5 d, 2 h 1.5 MAC isoflurane preconditioning can obviously reduce death of the hippocampal CA I pyramidal cells(P < 0.05 ). Conclusion Inhalation anesthetic isoflurane suppresses the apoptosis of neural cells following ischemia and induce neuroprotection. The JNK signal pathway probably mediates the neuroprotection of isoflurane to brain injured. Key words: ischemia/refusion;  isofluranc;  JNK signal pathway