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目的:观察α2肾上腺受体激动剂对大鼠体外循环（CPB）致脑损伤、核转录因子-κB（NF-κB）蛋白及炎性因子表达的影响。方法:成年清洁级健康雄性SD大鼠32只，按照随机数字表法分为4组：S组进行麻醉诱导及穿刺置管操作，机械通气60 min，不行CPB；C组建立CPB并持续60 min；A组CPB前30 min腹腔注入α2-AR激动剂右美托咪定25 μg/kg，建立CPB并持续60min；B组体外循环前30 min腹腔注入右美托咪定25 μg/kg+乙酰胆碱能受体拮抗剂甲基牛扁碱6 mg/kg，建立CPB持续60 min。CPB后2 h断头取右侧脑海马组织观察病理学结果。取左侧的海马组织免疫印迹法检测NF-κB/p65蛋白的表达。采血液标本ELISA法检测血清S100β、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的浓度。结果:S组海马锥体细胞形态正常完整，C组锥体细胞受损情况较重，核固缩，间隙增宽，A组受损较轻，仅见少量锥体细胞死亡，B组受损较A组重；C组、A组和B组S100β、IL-6和TNF-α水平均升高（n P<0.05）。与C组比较，A组S100β、IL-6和TNF-α水平降低（n P<0.05）。C组、A组和B组NF-κB/p65的表达升高（n P<0.05），与C组比较，A组NF-κB/p65表达降低（n P<0.05），B组NF-κB/p65表达高于C组、A组（n P<0.05）。n 结论:α2-AR激动剂能够调低CPB时NF-κB信号表达，减少炎性因子的释放，可能是α2-AR激动剂实现该保护作用的机制之一。“,”Objective:To investigate the effect of α2-adrenoceptor agonists on brain injury and the expression of nuclear factor-κB and inflammatory factors induced by cardiopulmonary bypass (CPB) in rats.Methods:Thirty-two clean male SD rats were randomly divided into four groups using a random number table. Group S was anesthetized, catheterized and mechanically ventilated for 60 minutes without CPB; groups A, B and C underwent CPB which was maintained for 60 minutes. Group A received the α2-AR agonist dexmedetomidine 25 μg/kg intraperitoneally 30 minutes before CPB; Group B received α2-AR agonist dexmedetomidine 25 μg/kg and acetylcholine receptor methylbovine 6 mg/kg intraperitoneally 30 minutes before CPB. At 2 h after CPB, the rats were decapitated and harvested for right hippocampus tissue sample which was subjected to pathological study. Western-blotting was used to detect the expression of NF-κB/p65 protein in left hippocampus sample. ELISA was used to detect the concentrations of serum S100β, IL-6 and TNF-α.Results:The morphology of the hippocampal pyramidal cells was normal in group S. The pyramidal cells in group C were more severely injured, with karyopyknosis and widened perinuclear space; group A showed slight damage of hippocampus tissue, with only a small amount of dead pyramidal cells; in group B, the tissue injury was more severe than that in group A. The levels of S100β, IL-6 and TNF-α were significantly increased in groups C, A and B (n P<0.05) . Compared with group C, the S100 β, IL-6 and TNF - α levels were decreased significantly in group A (n P<0.05) . The expression of NF-κB/p65 was higher in groups C, A and B (n P<0.05) . Compared with group C, the expression of NF-κB/p65 was decreased in group A (n P<0.05) . The expression of NF-κB/p65 in group B was higher compared with groups C and A (n P<0.05) .n Conclusions:α2-AR agonists can reduce the release of inflammatory factors by inhibiting the expression of NF-κB/p65 triggered by CPB. This may be one of the mechanisms via whichα2-AR agonists exhibit protective effects.