期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-06630-0
关键词
-
资金
- Ministry of Education, Culture, Sports, Science and Technology, Japan, KAKENHI [26740024, 26460139, 25340047]
- Mishima Kaiun Memorial Foundation
- SKYLARK Food Science Institute
- Tokushima Bunri University
- Grants-in-Aid for Scientific Research [26740024, 17K08356, 26460139] Funding Source: KAKEN
Several studies have shown that docosahexaenoic acid (DHA) attenuates epileptic seizures; however, the molecular mechanism by which it achieves this effect is still largely unknown. DHA stimulates the retinoid X receptor, which reportedly regulates the expression of cytochrome P450 aromatase (P450arom). This study aimed to clarify how DHA suppresses seizures, focusing on the regulation of 17 beta-estradiol synthesis in the brain. Dietary supplementation with DHA increased not only the expression of P450arom, but also 17 beta-estradiol in the cerebral cortex. While DHA did not affect the duration or scores of the seizures induced by pentylenetetrazole, DHA significantly prolonged the seizure latency. A P450arom inhibitor, letrozole, reduced 17 beta-estradiol levels and completely suppressed the elongation of seizure latency elicited by DHA. These results suggest that DHA delays the onset of seizures by promoting the synthesis of 17 beta-estradiol in the brain. DHA upregulated the expression of anti-oxidative enzymes in the cerebral cortex. The oxidation in the cerebral cortex induced by pentylenetetrazole was significantly attenuated by DHA, and letrozole completely inhibited this suppressive action. Thus, the anti-oxidative effects of 17 beta-estradiol may be involved in the prevention of seizures mediated by DHA. This study revealed that 17 beta-estradiol in the brain mediated the physiological actions of DHA.
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