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J. Biol. Chem., Vol. 278, Issue 44, 43807-43817, October 31, 2003
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Novel Docosanoids Inhibit Brain Ischemia-Reperfusion-mediated Leukocyte Infiltration and Pro-inflammatory Gene Expression*
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From the
Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112 and the ¶Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115
Ischemic stroke triggers lipid peroxidation and neuronal injury. Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte infiltration and pro-inflammatory gene expression also contribute to stroke damage. In this study using lipidomic analysis, we have identified stereospecific messengers from docosahexaenoate-oxygenation pathways in a mouse stroke model. Aspirin, widely used to prevent cerebrovascular disease, activates an additional pathway, which includes the 17R-resolvins. The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NF
B, and cyclooxygenase-2 induction in experimental stroke and elicited neuroprotection. In addition, in neural cells in culture, this lipid messenger also inhibited both interleukin 1-
-induced NFB activation and cyclooxygenase-2 expression. Thus, the specific novel bioactive docosanoids generated in vivo counteract leukocyte-mediated injury as well as pro-inflammatory gene induction. These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid is also the endogenous precursor to a neuroprotective signaling response to ischemia-reperfusion.
Received for publication, June 3, 2003 , and in revised form, August 14, 2003.
* This work was supported by the Neurobiotechnology Program of Louisiana, National Science Foundation Grant NSF/LEQSF(2001-2004)-RII-02, and National Institutes of Health Grants P20RR016816, NS23002 (to N. G. B.), AG18031 (to W. J. L.), GM38765 and P01DE13499 (to C. N. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
These authors and both laboratories contributed equally to this work.
|| To whom correspondence should be addressed: LSU Neuroscience Center of Excellence, 2020 Gravier St., Suite D, New Orleans, LA 70112. Tel.: 504-599-0832; Fax: 504-568-5801; E-mail: nbazan{at}lsuhsc.edu.
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