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目的：探讨十六酰胺乙醇（Palmitoylethanolamide PEA）对大鼠脑缺血再灌注损伤的保护作用及机制。方法：将雄性SD大鼠随机分为：假手术组、药物组、模型组。采用线栓法制造大脑中动脉缺血再灌注模型，药物组于缺血后30 分钟及再灌注后2小时给予PEA（10 mg/Kg）腹腔注射。于再灌注24 h后，对各组大鼠进行神经功能评分，TTC 染色法测脑梗死体积，硫代巴比妥法测丙二醛（MDA）含量，黄嘌呤氧化酶法测超氧化物歧化酶（SOD）活性，Western Blot 法测Bcl-2 和Bax 蛋白含量。结果：药物组神经功能评分均值为1.33± 0.49 分，而模型组为2.20± 0.41 分，药物组神经功能评分显著低于模型组（P<0.05）；药物组的脑梗死体积为 114.00± 8.63 mm3，而模型组脑梗死体积为243.40± 14.19 mm3，药物组脑梗死体积显著低于模型组（P<0.05）；药物组MDA 含量为3.85± 0.29 nmol/mg prot，SOD 活性为13.95± 0.71 U/mg prot，而模型组MDA 含量为4.85± 0.30 nmol/mg prot，SOD 活性为 12.44± 0.40 U/mg prot，与模型组相比，药物组的MDA 含量显著降低，而SOD活性显著增高（P<0.05）；药物组Bcl-2蛋白与β-action 蛋白的IOD 值比值为0.53± 0.013 %，Bax 蛋白与β-action 蛋白的IOD值比值为0.54± 0.012 %，模型组Bcl-2 蛋白与β-action 蛋白的IOD值比值为0.40± 0.012 %，Bax蛋白与茁-action 蛋白的IOD值比值为0.80± 0.012 %。药物组Bax 蛋白含量显著低于模型组（P<0.05），而Bcl-2蛋白含量显著高于模型组（P<0.05）。结论：PEA 对大鼠脑缺血再灌注损伤具有保护作用，可能是通过抗凋亡、抗氧化应激等作用实现。

英文摘要:

Objective:To test the protection effect of PEA and to explore the possible mechanism.Methods:The male SD rats were divided into three groups: sham operation group, model group and treatment group.The models of middle cerebral artery occlusion were established with the suture method. The rats of treatment group were received PEA (10 mg/kg i.p.) 30 min and 4h after ischemia. 24 h after the reperfusion, neurological deficit was scored, and then removed their brains. TTC staining was applied to quantify infarction volume, Xanthine oxidase method was usedto test the activity of SOD and the malondialdehyde (MDA) content were measured by the method of thiobarbituric acid reaction (TBA). The protein of Bcl-2 and Bax were tested by Western Blot analysis.Results:In our study, neurological function score of treatment group was 1.33± 0.49, and model group's was 2.20± 0.41. And we also measured the infarct volume of model group(243.40± 14.19 mm3) and treatment group(114.00± 8.63 mm3). So cmpared with model group, the neurological deficit scores and infarction volume of treatment group were significantly decreased (P<0.05). The MDA content of treatment group was 3.85± 0.29 nmol/mg prot, and model group's was 4.85± 0.30nmol/mg prot. The SOD activity of treatment group was 13.95± 0.71 U/mg prot, and model group's was 12.44± 0.40 U/mg prot. So compared with model group, the activity of SOD of treatment group increased significantly and the content of MDA decreased (P<0.05). In the treatment group, the ratio of Bcl-2 protein content to β-action protein content was 0.53± 0.013 %, and the ratio of Bax protein content to β-action protein content was 0.54± 0.012 %. In the model group, the ratio of Bcl-2 protein content to β-action protein content was 0.40± 0.012 %,and the ratio of Bax protein content to β-action protein content was 0.80± 0.012 %. Compared with model group, the content of bcl-2 in treatment group increased significantly and the content of Bax was decreased significantly (P<0.05).Conclusion:The cerebral ischemia reperfusion injury was significantly reduced by PEA administration. PEA had the protect effect on cerebral ischemia reperfusion fromantioxidant and anti-apoptosis.

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