Abstract: A relationship between status epilepticus (SE) and oxidative stress has recently begun to be recognized. To explore whether the flavonoids extracted from licorice (LFs) have any protective effect on kainate (KA)-induced seizure in mice, we treated mice with LFs before and after KA injection. In KA-treated mice, we found that superoxide dismutase (SOD) activity decreased immediately after the onset of seizure at 1 h and then increased at 6 h. It returned to baseline 1 d after seizure and then increased again at 3, 7, and 28 d, while malondialdehyde (MDA) content remained at a high level at 1 h, 6 h, 3 d, 7 d, and 28 d, indicating a more oxidized status related to the presence of more reactive oxygen species (ROS). Treatment with LFs before KA injection reversed the seizure-induced change in SOD activity and MDA content at 1 h, 6 h, 3 d, 7 d, and 28 d. Treatment with LFs after seizure decreased KA-induced SOD activity and MDA content at 7 and 28 d. Also, LF pre- and post-KA treatments decreased seizure-induced neuronal cell death. Subsequently, Morris water maze tests revealed that the escape latency was significantly decreased and the number of target quadrant crossings was markedly increased in the LF-treated groups. Thus, our data indicate that LFs have protective effects on seizure-induced neuronal cell death and cognitive impairment through their anti-oxidative effects.

Key words: Seizure, Kainate, Flavonoid, Licorice, Antioxidant, Malondialdehyde (MDA), Superoxide dismutase (SOD)

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