Abstract: To explore the effects of Cilostazol on the learning and recalling ability and caspase-3 expression after global cerebral ischemia-reperfusion in rats. MethodsTransient global cerebral ischemia was induced by the fourvessel occlusion in SpragueDawley(SD) rats.SD rats were randomly divided into sham-operated group（n=8×1）, model group(n=8×7) and Cilostazol-treating group(n=8×7). Rats in treatment group received two oral administration of cilostazol at 6h and 2h before the global cerebral ischemia，then they were given cilostazol every 24h.　Rats in other groups were given the same volume of 30% dimethyl sulfoxide. The rats in model control group and treatment group were decapitated at 6、12、24、48、72h、5d and 7d after 10min cerebral ischemia. The expression of caspase3 in CA1 region of hippocampus were detected by the method of immunohistochemistry. The another 24 rats were randomly divided into 3 groups:shamoperated group(n=8), ischemia reperfusion group (n=8)　and treatment group(n=8).　They were used to study the learning and recalling ability of rats at 7?d after global ischemia-reperfusion by Morris water maze.Results Caspase-3 was scarecely expressed in shamoperated group；while in model group, it increased at 6 hour, peaked at 72 hour, and deceased nearby to the base lever at 7 day；for caspase-3 mean positive cells in CA1 region, they were obviously lower in 48、72?h、5?d　and 7?d subgroups of treatment group than those in model group（P＜0.05）. Within 5 days, the Escape Latency(EL) in ischemia reperfusion group and treatment group was markedly longer than that of in shamoperated group(P＜0.01, P＜0.05 respectively)；within 4 days, the Escape Latency(EL) in treatment group was markedly shorter than that of in ischemia reperfusion group(P＜0.01);whereas on the fifth day,there was no significant difference in these two groups.Conclusion Cilostazol can effectively inhibited the increase of caspase3 levels which may be one mechanism of its increasing the learning and recalling ability of rats.

Key words: phosphodiesterase inhibitors, IschemiaHypoxia, Brain, Reperfusion Injury, Caspase-3