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- Title
Alleviation of Kainic Acid-Induced Brain Barrier Dysfunction by 4-O-Methylhonokiol in In Vitro and In Vivo Models.
- Authors
Han, Jin-Yi; Ahn, Sun-Young; Yoo, Jae Hyeon; Nam, Sang-Yoon; Hong, Jin Tae; Oh, Ki-Wan
- 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 4×109 M-1·S-1, 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.
- Subjects
REACTIVE oxygen species; ANIMAL experimentation; BIOPHYSICS; BLOOD-brain barrier; BRAIN; CELL culture; RESEARCH methodology; MICE; RESEARCH funding; WESTERN immunoblotting; MALONDIALDEHYDE; PLANT extracts; IN vitro studies; ONE-way analysis of variance
- Publication
BioMed Research International, 2015, Vol 2015, p1
- ISSN
2314-6133
- Publication type
Article
- DOI
10.1155/2015/893163