| Objective: To investigate the temporal expression of AQP4 and GLT1 in rat brain after focal ischemia and discuss the correlation of AQP4 and GLT1 expression with astocytic gliosis and neuronal damage following ischemia.Methods: (1) Rat were indued focal ischemia by transient middle cerebral artery occlusion (MCAO). And the rats were sacrificed respectively at 6h, 24h, 3d, 7d, after MCAO. (2)The expressions of AQP4 and GLT1 on astrocytes in cerebral cortex and hippocampal regions were detected by immunofluorescence analysis; The infarct volume was measured by TTC staining; and the apoptosis of neuron after cerebral ischemia and reperfusion was determined by TUNEL method.Results:(1)The ischemic infarction could be observed at 6h after MCAO group, which increased significantly at 24h.(2)Compared with control and sham groups, at 6h after ischemia, TUNEL positive cells could be detected in cortex and hippocampus , which increased gradually after that and peaked at 3 d.(3)Compared with control and sham groups, the expression of GLT1 significantly increased in the cortex after cerebral ischemia/reperfusion at 24h, ,72h and 7d. But the expression of GLT1 in himpocampus decreased at 6h significantly, which further declined at 24h and maintained stable at 72h and 7d after MCAO.(4)Compared with control and sham groups, the expression of GFAP were increased significantly at 24 h and continued to increase at 72h and 7d.following MCAO(5)Compared with control and sham groups, expression of AQP4 in cerebral ischemia were slightly decreased at 6 h whereas increased significantly at 24h ,72h and 7d in the hippocampus. Conclusion :(1) Ischemic infarction appeared at 6h after MCAO. The neural apoptosis significantly increased at 24h in the cortex and hippocampus. (2) The compromised expression of GLT1 might be attributable for the neuronal apoptosis in hippocampus. (3) GFAP and GLT1 expression shows the similar trend after MCAO, suggesting that GLT1 expression is related to astrogliosis. (4) The expression of AQP4 increased after MCAO, suggesting it may also be involved in neuronal injury in the cortex and the hippocampus. |