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