Abstract
BackgroundIschemia/reperfusion leads to inflammation and oxidative stress which damages membrane highly polyunsaturated fatty acids (HPUFAs) and eventually induces neuronal death. This study evaluates the effect of the administration of Pistacia lentiscus L. essential oil (E.O.), a mixture of terpenes and sesquiterpenes, on modifications of fatty acid profile and endocannabinoid (eCB) congener concentrations induced by transient bilateral common carotid artery occlusion (BCCAO) in the rat frontal cortex and plasma.MethodsAdult Wistar rats underwent BCCAO for 20 min followed by 30 min reperfusion (BCCAO/R). 6 hours before surgery, rats, randomly assigned to four groups, were gavaged either with E.O. (200 mg/0.45 ml of sunflower oil as vehicle) or with the vehicle alone.ResultsBCCAO/R triggered in frontal cortex a decrease of docosahexaenoic acid (DHA), the membrane highly polyunsaturated fatty acid most susceptible to oxidation. Pre-treatment with E.O. prevented this change and led further to decreased levels of the enzyme cyclooxygenase-2 (COX-2), as assessed by Western Blot. In plasma, only after BCCAO/R, E.O. administration increased both the ratio of DHA-to-its precursor, eicosapentaenoic acid (EPA), and levels of palmytoylethanolamide (PEA) and oleoylethanolamide (OEA).ConclusionsAcute treatment with E.O. before BCCAO/R elicits changes both in the frontal cortex, where the BCCAO/R-induced decrease of DHA is apparently prevented and COX-2 expression decreases, and in plasma, where PEA and OEA levels and DHA biosynthesis increase. It is suggested that the increase of PEA and OEA plasma levels may induce DHA biosynthesis via peroxisome proliferator-activated receptor (PPAR) alpha activation, protecting brain tissue from ischemia/reperfusion injury.
Highlights
Ischemia/reperfusion leads to inflammation and oxidative stress which damages membrane highly polyunsaturated fatty acids (HPUFAs) and eventually induces neuronal death
Reperfusion of neural ischemic tissue is desirable, the post-ischemic reestablishment of blood supply leads to a general impairment of translation capability, oxidative stress and free radical formation which can eventually cause neuronal death [6,7,8]
Neuronal membranes are rich in highly polyunsaturated fatty acids (HPUFAs) which serve as reservoirs of biologically active lipids in physiological conditions, whereas, in stressful circumstances, are target of free radical-mediated lipid peroxidation whose products, in turn, can injure the brain [9,10,11]
Summary
Ischemia/reperfusion leads to inflammation and oxidative stress which damages membrane highly polyunsaturated fatty acids (HPUFAs) and eventually induces neuronal death. Reperfusion of neural ischemic tissue is desirable, the post-ischemic reestablishment of blood supply leads to a general impairment of translation capability, oxidative stress and free radical formation which can eventually cause neuronal death [6,7,8]. Neuronal membranes are rich in highly polyunsaturated fatty acids (HPUFAs) which serve as reservoirs of biologically active lipids in physiological conditions, whereas, in stressful circumstances, are target of free radical-mediated lipid peroxidation whose products, in turn, can injure the brain [9,10,11]. The main products of lipid peroxidation are fatty acid hydroperoxides which are quite unstable and capable to propagate free radical reactions, extending the damage [13]
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