Alpha-tocopherol Prevents H2O2-induced Tight Junction Occludin Disruption in Blood-Brain Barrier.
10.11637/kjpa.2006.19.3.223
- Author:
Hee Sang LEE
1
;
Kee NAMKOONG
;
Ki Hwan YOOK
;
Jun Seok AHN
;
Maeng Seok NOH
;
Dae Jin KIM
;
Yoon Hee CHUNG
;
Sung Su KIM
;
Won Bok LEE
;
Kyung Yong KIM
Author Information
1. Department of Anatomy, College of Medicine, Chung-Ang University, Korea. skull@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Alpha-tocopherol;
BBB;
Tight junction;
Occludin;
H2O2
- MeSH:
alpha-Tocopherol*;
Animals;
Blood-Brain Barrier*;
Blotting, Western;
Brain;
Cell Survival;
Endothelial Cells;
Humans;
Microscopy, Confocal;
Microscopy, Phase-Contrast;
Microvessels;
Neurodegenerative Diseases;
Occludin*;
Rats;
Reactive Oxygen Species;
Tight Junctions*;
Vitamin E;
Vitamins
- From:Korean Journal of Physical Anthropology
2006;19(3):223-233
- CountryRepublic of Korea
- Language:English
-
Abstract:
Vitamin E is the most important lipid-soluble antioxidant in humans. Although alpha-tocopherol is suggested that it has protective effect from many diseases, little is known about the prevention of occludin alteration in tight junction of blood-brain barrier (BBB) under pathologic insults producing reactive oxygen species (ROSs). In this study, the effects of alpha-tocopherol on H2O2-induced tight junction occludin were studied. Primary culture of rat brain microvessel endothelial cells was investigated with confocal microscopy, Western blot, and cell viability assay. Alpha-tocopherol had no apparent cytotoxicity up to 2.8 mM. The preincubation with alpha-tocopherol suppressed the H2O2-induced cytotoxicity in Alamar Blue assay and phase contrast microscopy. In confocal laser microscopy and Western blot, H2O2-induced loss of occludin was suppressed by preincubation with alpha-tocopherol. The present findings provide evidence that alpha-tocopherol may be beneficial for cellular protection from pathologic insults. Since alpha-tocopherol was demonstrated to have far fewer adverse effects, it would become a noteworthy nutrient or drug for the treatment of neurodegenerative diseases.