Decursin attenuates kainic acid-induced seizures in mice

Jong Keun Lee, Ji Woon Jeong, Taeik Jang, Go Woon Lee, Hogyu Han, Jae Seon Kang, Ik Hwan Kim

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


Epilepsy is a neurological disorder with recurrent unprovoked seizures as the main symptom. Of the coumarin derivatives in Angelica gigas, decursin, a major coumarin component, was reported to exhibit significant protective activity against glutamate-induced neurotoxicity when added to primary cultures of rat cortical cells. This study served to investigate the effects of decursin on a kainic acid (KA)-induced status epilepticus model. Thirty minutes after intraperitoneal injections of decursin (20 mg/kg) in male 7-week-old C57BL/6 mice, the animals were treated with KA (30 mg/kg, intraperitoneally) and then examined for behavioral seizure score, electroencephalogram, seizurerelated expressed protein levels, neuronal cell loss, neurodegeneration, and astrogliosis. KA injections significantly enhanced neurodegenerative conditions but treatment with decursin 30 min before KA injection reduced the detrimental effects of KA in mice. The decursin-treated KA-injected group showed significantly decreased behavioral seizure activity and remarkably attenuated intense and high-frequency seizure discharges in the parietal cortex for 2 h compared with the group treated only with KA. Furthermore, in-vivo results indicated that decursin strongly inhibits selective neuronal death, astrogliosis, and oxidative stress induced by KA administration. Therefore decursin is able to attenuate KA-induced seizures and could have potential as an antiepileptic drug. NeuroReport 25:1243-1249

Original languageEnglish
Pages (from-to)1243-1249
Number of pages7
Issue number16
Publication statusPublished - 2014 Jan 1

ASJC Scopus subject areas

  • General Neuroscience


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