Korean J Physiol Pharmacol.  2018 Jan;22(1):63-70. 10.4196/kjpp.2018.22.1.63.

Cilostazol attenuates kainic acid-induced hippocampal cell death

Affiliations
  • 1Department of Neurosurgery, Institute of Health Sciences, Gyeongsang National University Changwon Hospital, Changwon 51472, Korea.
  • 2Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea. anaroh@gnu.ac.kr
  • 3Department of Neurosurgery, Institute of Health Sciences, Gyeongsang National University Hospital, Gyeongsang National University College of Medicine, Jinju 52727, Korea. gnuhpis@gnu.ac.kr

Abstract

Cilostazol is a selective inhibitor of type 3 phosphodiesterase (PDE3) and has been widely used as an antiplatelet agent. Cilostazol mediates this activity through effects on the cyclic adenosine monophosphate (cAMP) signaling cascade. Recently, it has attracted attention as a neuroprotective agent. However, little is known about cilostazol's effect on excitotoxicity induced neuronal cell death. Therefore, this study evaluated the neuroprotective effect of cilostazol treatment against hippocampal neuronal damage in a mouse model of kainic acid (KA)-induced neuronal loss. Cilostazol pretreatment reduced KA-induced seizure scores and hippocampal neuron death. In addition, cilostazol pretreatment increased cAMP response element-binding protein (CREB) phosphorylation and decreased neuroinflammation. These observations suggest that cilostazol may have beneficial therapeutic effects on seizure activity and other neurological diseases associated with excitotoxicity.

Keyword

Cilostazol; Hippocampus; Kainic acid; Neuroinflammation; Neuronal death
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