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BioMed Research International
Volume 2015, Article ID 893163, 14 pages
http://dx.doi.org/10.1155/2015/893163
Research Article

Alleviation of Kainic Acid-Induced Brain Barrier Dysfunction by 4-O-Methylhonokiol in In Vitro and In Vivo Models

1Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju 361-763, Republic of Korea
2Lee’s Biotech Co., Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-606, Republic of Korea
3College of Pharmacy, Chungbuk National University, Cheongju 361-763, Republic of Korea
4College of Veterinary Medicine, Chungbuk National University, Cheongju 361-763, Republic of Korea

Received 22 April 2014; Revised 6 August 2014; Accepted 11 August 2014

Academic Editor: Yiying Zhang

Copyright © 2015 Jin-Yi Han et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This experiment was designed to investigate whether 4-O-methylhonokiol (MH), a principal ingredient of Magnolia (M.) officinalis bark, alleviated acute intraperitoneal (i.p.) kainic acid- (KA-) induced brain blood barrier dysfunction (BBBD) via pathological examination and cytological analyses of the brain tissues of mice. KA (10–30 mg/kg) time- and dose-dependently increased the water content of brain tissues and induced edema and encephalopathy. However, pretreatment with MH (5 and 20 mg/kg, i.p.) significantly reduced the water content of the brain compared to that observed in the KA control group. Furthermore, MH significantly and dose-dependently reversed the remarkable variations in evan’s blue dye (EBD) staining and malondialdehyde (MDA) levels that were induced by KA (10 mg/kg, i.p.). MH also decreased the elevated seizure scores that were induced by KA (10 mg/kg, i.p.) in mice in a manner similar to scavengers such as DMTU and trolox. Additionally, MH significantly scavenged intracellular ROS and Ca2+ within hippocampal cells. The tight junction seals mediated by claudin (Cld-5) were also found to be modulated by MH. MH efficiently reduced 1,1-diphenyl-2-picrylhydrazyl (DPPH) (IC50, 52.4 mM) and OH with an electron spin resonance (ESR) signal rate constant of , which is close to the reactivity of the vitamin E analog trolox. Taken together, these results suggest that MH may enhance radical scavenging in lipid and hydrophobic environments, which may be important for the physiological activity of the barrier.