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目的:观察δ-阿片受体激动剂 DADLE([D-Ala2,D-Leu5]enkephali)对大鼠急性全脑缺血再灌注后海马区神经元 ERK 信号通路和 Caspase-3表达的影响.方法:将50只 SD 大鼠随机分为5组:假手术组(Sham)、模型组(I/R)、DADLE 处理组(根据不同剂量可分为2 mg/kg[A]、3 mg/kg[B]、5 mg/kg[C]).采用改良的二血管阻断加低血压法建立全脑缺血再灌注模型.于缺血15 min 后经颈外静脉注射 DADLE 并于再灌注120 min 后处死.开颅取其新鲜海马组织,采用 western blot 检测海马组织 Caspase-3的表达,以及采用免疫组织化学法检测非磷酸化 ERK 与磷酸化 ERK(P-ERK)的表达状况.结果:Sham 组 ERK 和 P-ERK 蛋白表达水平显著低于其他各组(P<0.05), DADLE 处理组与 I/R 组相比,其 ERK 和 P-ERK 蛋白的表达量明显上调(P<0.05).海马组织 Caspase-3蛋白表达 I/R 组较 Sham 组表达明显上调(P<0.05),而 DADLE 处理组与 IR 组比较,海马组织 Caspase-3蛋白表达明显下降(P<0.05).结论:DADLE 对大鼠急性全脑缺血再灌注后海马区神经元有保护作用,说明 DADLE 可通过上调 ERK 信号通路以及抑制 Caspase-3的表达而起到保护脑组织的作用.“,”Objective:To observe the effects of δ-opioid receptor agonist DADLE([D-Ala2,D-Leu5]enkephali)on expression of ERK signaling pathway and Caspase-3 following cerebral ischemia-reperfusion in hippocampus of rat. Method:In total,50 SD rats were randomly divided into 5 groups:a sham-operated,a I/R and three DADLE-treated(different drug doses:2 mg/kg[A],3 mg/kg[B] and 5 mg/kg[C]).Use improvement of two vessels occlusion add hypotension to establish the global cerebral ischemia/reperfusion model in rats.Injecting DADLE through external jugular vein after ischemic 15 min,and the rats were respectively killed after reperfusion 120min.The expression of Caspase-3 were detected by Western blot,and the expression of non-phosphorylated ERK and phosphorylation of ERK(P-ERK)were detected by Immunohistochemistry assay. Result:The expression of ERK and P-ERK was lower in the Sham group than in the others(P<0.05),and compared with I/R group,the expression of ERK and P-ERK of each DADLE-treated group was higher obviously(P<0.05). The expression of Caspase-3 in hippocampus was higher in the I/R group than in the Sham group, and compared with I/R group,the expression of Caspase-3 of each DADLE-treated group was lower obviously(P<0.05). Conclusion:DADLE may be have some protective effects on neurons in hippocampus after the global cerebral ischemia/reperfusion in rats,and it related. Shows that DADLE can play a role in protecting brain tissue by increasing the expression of ERK signaling pathway and inhibiting the expression of Caspase-3.