-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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Kilaru et al. (2011) studied this question.
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