Department of Biomedical Sciences, University of Cagliari, Cittadella Universitaria, Monserrato, Italy.
Lipids Health Dis. 2012 Jan 12;11:8. doi: 10.1186/1476-511X-11-8.
Ischemia/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.
Adult 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.
BCCAO/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).
Acute 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.
缺血/再灌注导致炎症和氧化应激，损伤膜高度多不饱和脂肪酸（HPUFAs），最终诱导神经元死亡。本研究评估了乳香精油（E.O.）的给药对大鼠前额皮质和血浆中由短暂双侧颈总动脉闭塞（BCCAO）引起的脂肪酸谱和内源性大麻素（eCB）同系物浓度变化的影响。
成年 Wistar 大鼠行 BCCAO 20 分钟，再灌注 30 分钟（BCCAO/R）。在手术前 6 小时，大鼠随机分为四组，分别灌胃给予 E.O.（200 mg/0.45 ml 葵花籽油作为载体）或单独给予载体。
BCCAO/R 在前额皮质中触发二十二碳六烯酸（DHA）的减少，DHA 是最易氧化的膜高度多不饱和脂肪酸。E.O.预处理可防止这种变化，并进一步导致环氧合酶-2（COX-2）水平降低，通过 Western Blot 评估。在血浆中，只有在 BCCAO/R 后，E.O.的给药才会增加 DHA 与其前体二十碳五烯酸（EPA）的比值，以及棕榈酰乙醇酰胺（PEA）和油酰乙醇酰胺（OEA）的水平。
在 BCCAO/R 之前进行急性 E.O.治疗会引起前额皮质的变化，其中 BCCAO/R 诱导的 DHA 减少明显得到预防，COX-2 表达减少，以及血浆中 PEA 和 OEA 水平和 DHA 生物合成增加。据推测，PEA 和 OEA 血浆水平的增加可能通过过氧化物酶体增殖物激活受体（PPAR）α的激活诱导 DHA 生物合成，从而保护脑组织免受缺血/再灌注损伤。
