alexa Changes in N-acylethanolamine Pathway Related Metabolites in a Rat Model of Cerebral Ischemia/Reperfusion
ISSN: 2153-0637

Journal of Glycomics & Lipidomics
Open Access

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Research Article

Changes in N-acylethanolamine Pathway Related Metabolites in a Rat Model of Cerebral Ischemia/Reperfusion

Aruna Kilaru1,,#, Pamela Tamura2#, Puja Garg3,4#, Giorgis Isaac2,§, David Baxter1, R. Scott Duncan3,4, Ruth Welti2, Peter Koulen1,3,4, Kent D.Chapman1 and Barney J. Venables1*

1University of North Texas, Center for Plant Lipid Research, Department of Biological Sciences, Denton, TX 76203

2Kansas State University, Kansas Lipidomics Research Center, Division of Biology, Manhattan, KS 66506

3University of Missouri – Kansas City, School of Medicine, Vision Research Center, Kansas City, MO 64108

4University of Missouri – Kansas City, School of Medicine, Departments of Basic Medical Science and Ophthalmology, Kansas City, MO 64108

#equal contribution

current address: Michigan State University, Department of Plant Biology, East Lansing, MI 48824

§current address: Pacific Northwest National Laboratory, PO Box 999, MSIN: K8-98, Richland, WA 99352

*Corresponding Author:
Dr. Barney J. Venables
University of North Texas, Center for Plant Lipid Research, Department of Biological Sciences, Denton
TX 76203,1155 Union Circle #305220
Phone 940-369-7708
Fax 940-565-4297
E-mail:[email protected]

Received date: October 08, 2010; Accepted date: November 16, 2010; Published date: November 18, 2010

Citation: Kilaru A, Tamura P, Garg P, Isaac G, Baxter D, et al. (2011) Changes in N-acylethanolamine Pathway Related Metabolites in a Rat Model of Cerebral Ischemia/Reperfusion. J Glycom Lipidom 1:101. doi: 10.4172/2153-0637.1000101

Copyright: © 2011 Kilaru A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



In mammals, the endocannabinoid signaling pathway provides protective cellular responses to ischemia. Previous work demonstrated increases in long-chain N -acylethanolamines (NAE) in ischemia and suggested a protective role for NAE. Here, a targeted lipidomics approach was used to study comprehensive changes in the molecular composition and quantity of NAE metabolites in a rat model of controlled brain ischemia. Changes of NAE, its precursors, N -acylphosphatidylethanolamines (NAPE), major and minor phospholipids and free fatty acids (FFA) were quantified in response to ischemia. The effect of intraperitoneal injection of N -palmitoylethanolamine (NAE 16:0) prior to ischemia on NAE metabolite and phospholipid profiles was measured. While ischemia, in general, resulted in elevated levels of N -acyl 16:0 and18:0 NAE, NAPE and FFA species, pretreatment with NAE 16:0 reduced infarct volume, neurological behavioral deficits in rats and FFA content in ischemic tissues. Pretreatment with NAE 16:0 did not affect the profiles of other NAE metabolites. These studies demonstrate the utility of a targeted lipidomics approach to measure complex and concomitant metabolic changes in response to ischemia. They suggest that the neuroprotective effects of exogenous NAE 16:0 and the reduction in inflammatory damage may be mediated by factors other than gross changes in brain NAE levels, such as modulation of transcriptional responses.

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