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The N‐acylethanolamines (NAEs) and 2‐arachidonoylglycerol (2‐AG) are bioactive lipids that can modulate inflammatory responses and protect neurons against glutamatergic excitotoxicity. We have used a model of focal cerebral ischemia in young adult mice to investigate the relationship between focal cerebral ischemia and endogenous NAEs. Over the first 24 h after induction of permanent middle cerebral artery occlusion, we observed a time‐dependent increase in all the investigated NAEs, except for anandamide. Moreover, we found an accumulation of 2‐AG at 4 h that returned to basal level 12 h after induction of ischemia. Accumulation of NAEs did not depend on regulation of N‐acylphosphatidylethanolamine‐hydrolyzing phospholipase D or fatty acid amide hydrolase. Treatment with the fatty acid amide hydrolase inhibitor URB597 (cyclohexyl carbamic acid 3′‐carbamoyl‐biphenyl‐3‐yl ester; 1 mg …