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Original Article

Exp Neurobiol 2017; 26(5): 266-277

Published online October 31, 2017

© The Korean Society for Brain and Neural Sciences

Beneficial Effects of Silibinin Against Kainic Acidinduced Neurotoxicity in the Hippocampus in vivo

Sehwan Kim1†, Un Ju Jung2†, Yong-Seok Oh3†, Min-Tae Jeon1, Hyung-Jun Kim4, Won-Ho Shin5, Jungwan Hong6* and Sang Ryong Kim1,6*

1School of Life Sciences, BK21 plus KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, 2Department of Food Science and Nutrition, Pukyong National University, Busan 48513, 3Department of Brain-Cognitive Science, Daegu-Gyeongbuk Institute of Science and Technology, Daegu 42988, 4Department of Neural Development and Disease, Department of Structure & Function of Neural Network, Korea Brain Research Institute, Daegu 41062, 5Predictive Model Research Center, Korea Institute of Toxicology, Daejeon 34114, 6Brain Science and Engineering Institute, Kyungpook National University, Daegu 41944, Korea

Correspondence to: *To whom correspondence should be addressed.
Sang Ryong Kim
TEL: 82-53-950-7362, FAX: 82-53-943-2762, e-mail:
Jungwan Hong
TEL: 82-53-950-7362, FAX: 82-53-943-2762, e-mail:
These authors contributed equally to this work.

Received: August 3, 2017; Revised: September 21, 2017; Accepted: October 5, 2017


Silibinin, an active constituent of silymarin extracted from milk thistle, has been previously reported to confer protection to the adult brain against neurodegeneration. However, its effects against epileptic seizures have not been examined yet. In order to investigate the effects of silibinin against epileptic seizures, we used a relevant mouse model in which seizures are manifested as status epilepticus, induced by kainic acid (KA) treatment. Silibinin was injected intraperitoneally, starting 1 day before an intrahippocampal KA injection and continued daily until analysis of each experiment. Our results indicated that silibinin-treatment could reduce seizure susceptibility and frequency of spontaneous recurrent seizures (SRS) induced by KA administration, and attenuate granule cell dispersion (GCD), a morphological alteration characteristic of the dentate gyrus (DG) in temporal lobe epilepsy (TLE). Moreover, its treatment significantly reduced the aberrant levels of apoptotic, autophagic and pro-inflammatory molecules induced by KA administration, resulting in neuroprotection in the hippocampus. Thus, these results suggest that silibinin may be a beneficial natural compound for preventing epileptic events.

Keywords: Silibinin, Epilepsy, Granule cell dispersion, Kainic acid, Neuroprotection