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Cilostazol attenuates kainic acid-induced hippocampal cell death
The Korean Journal of Physiology and Pharmacology ; : 63-70, 2018.
Artículo en Inglés | WPRIM | ID: wpr-727937
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.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Fosforilación / Convulsiones / Adenosina Monofosfato / Muerte Celular / Proteína de Unión a Elemento de Respuesta al AMP Cíclico / Fármacos Neuroprotectores / Usos Terapéuticos / Hipocampo / Ácido Kaínico / Neuronas Tipo de estudio: Estudio pronóstico Límite: Animales Idioma: Inglés Revista: The Korean Journal of Physiology and Pharmacology Año: 2018 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Fosforilación / Convulsiones / Adenosina Monofosfato / Muerte Celular / Proteína de Unión a Elemento de Respuesta al AMP Cíclico / Fármacos Neuroprotectores / Usos Terapéuticos / Hipocampo / Ácido Kaínico / Neuronas Tipo de estudio: Estudio pronóstico Límite: Animales Idioma: Inglés Revista: The Korean Journal of Physiology and Pharmacology Año: 2018 Tipo del documento: Artículo