Cilostazol increases the level of intracellular cyclic adenosine monophosphate (cAMP) by inhibiting cyclic nucleotide phosphodiesterase-3. Its main role was induced by the increased cAMP, including the inhibition of platelet aggregation, anti-thrombosis, vasodilation, and anti-endothelial cell proliferation. Recent experimental studies line indicated that cilostazol is promising in the intervention of acute cerebral ischemia and chronic cerebral hypoperfusion. Clinical trials have also demonstrated its efficacy. This article summarizes the pharmacological effect and mechanism of cilostazol, as well as its protective effect during ischemic stroke.