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Objective:Water homeostasis in the brain has the clinical importance. Facilitation of water molecules through aquaporins(AQP) known as a water channel family, may contribute to brain edema formation. Cerebral edema following cerebral ischemia is a final common pathway of numerous neurological disorders. However, little is known about the molecular mechanisms responsible for the alteration of cerebral water balance. We present the changes of AQP expression in cerebral edema following focal cerebral ischemia. Methods : Cerebral ischemia was induced by permanent middle cerebral artery(MCA) occlusion in rats and estimated by the discoloration after triphenyltetrazoliumchloride immersion. The changes of AQP1 and AQP4 expression were evaluated using western blot and confocal microscopy. Results : MCA occlusion resulted in well-demarcated infarct at 4 hours, which enlarged with time but declined after 3 days. The AQP1 expression of infarcted hemisphere was down-regulated, but became to recover after 3 days. The expression of vascular endothelial growh factor was increased as early as 4 hours after MCA occlusion, and returned to the baseline level after 3 days. The AQP4 expression was upregulated after 4 hours, and remained high up to 7 days. The AQP4 immunostaining was specifically increased in the gliofibrillary astrocytes around the infarct area, ventricles and blood vessels. Conclusion : These results indicate the important role of AQP1 and AQP4 in the formation and resolution of brain edema induced by cerebral ischemia, and provide the potential target for the new therapeutic strategy of cerebral edema. Key words:Brain edema;Brain ischemia;Middle cerebral artery;AQP1;AQP4.