Cilostazol attenuates kainic acid-induced hippocampal cell death.
10.4196/kjpp.2018.22.1.63
- Author:
Young Seop PARK
1
;
Zhen JIN
;
Eun Ae JEONG
;
Chin ok YI
;
Jong Youl LEE
;
In Sung PARK
;
Gu Seob ROH
Author Information
1. Department of Neurosurgery, Institute of Health Sciences, Gyeongsang National University Changwon Hospital, Changwon 51472, Korea.
- Publication Type:Original Article
- Keywords:
Cilostazol;
Hippocampus;
Kainic acid;
Neuroinflammation;
Neuronal death
- MeSH:
Adenosine Monophosphate;
Animals;
Cell Death*;
Cyclic AMP Response Element-Binding Protein;
Hippocampus;
Kainic Acid;
Mice;
Neurons;
Neuroprotective Agents;
Phosphorylation;
Seizures;
Therapeutic Uses
- From:The Korean Journal of Physiology and Pharmacology
2018;22(1):63-70
- CountryRepublic of Korea
- Language:English
-
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.
