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Journal of Lipid Research, Vol. 44, 1984-1991, October 2003
Copyright © 2003 by American Society for Biochemistry and Molecular Biology


* Department of Psychiatry, University of British Columbia, Canada
Brain and Behaviour Research Institute, Academic Hospital Maastricht, University of Maastricht, The Netherlands
Laxdale Research, Stirling, Scotland, UK
1 To whom correspondence should be addressed. e-mail: caisong{at}interchange.ubc.ca
The present study demonstrated that an
(n)-3 fatty acid, ethyl-eicosapentaenoic acid (ethyl-EPA), supplemented diet significantly attenuated the stress/anxiety behavior of rats in the "open field" and elevated plus maze, which was induced by subchronic intracerebroventricular administration of proinflammatory cytokine interleukin (IL)-1ß. Ethyl-EPA also reduced the rise in serum corticosterone induced by IL-1. The n-6 fatty acid ethyl-
-linolenic acid (ethyl-GLA) had little effect on the IL-1-induced changes in behavior and the corticosterone concentration. Following IL-1ß administration, ethyl-EPA reduced the elevated prostaglandin (PG) E2 secretion and increased the secretion of antiinflammatory cytokine IL-10 from whole blood cells. Ethyl-GLA showed a similar antiinflammatory effect to ethyl-EPA. By contrast, n-6 fatty acid arachidonic acid (AA) had no effect on the behavior, immune, and endocrine changes induced by IL-1. AA alone enhanced the basal inflammatory response, raised serum corticosterone concentrations, and induced anxiety behavior in the elevated plus maze. The reduced growth rates of rats following the administration of IL-1 was attenuated by ethyl-EPA, and to a greater extent by ethyl-EPA plus ethyl-GLA, but not by AA alone or in combination with ethyl-EPA.
Thus, ethyl-EPA would appear to antagonise the endocrine, immune, and behavioral effects of subchronic IL-1 administration. Ethyl-GLA only antagonised IL-1-induced inflammatory changes, whereas AA caused an increase in the secretion of corticosterone and PGE2, and induced anxiety-like behavior without enhancing the effects of IL-1.
Abbreviations: AA, arachidonic acid; EPA, eicosapentaenoic acid; GLA,
-linolenic acid; IL, interleukin; PGE2, prostaglandin E2
Supplementary key words eicosapentaenoic acid
-linolenic acid arachidonic acid phospholipid supplementation open field inflammation prostaglandin E2 interleukin-10
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