目的:评价海马miR-153在电针预处理减轻大鼠脑缺血再灌注损伤中的作用。方法:清洁级健康雄性SD大鼠150只，8～12周龄，体重200～250 g，采用随机数字表法分为5组(n n＝30)：对照组(C组)、脑缺血再灌注组(I/R组)、假电针组(S组)、电针百会穴预处理组(E组)和miR-153激活剂组(A组)。I/R组采用线栓法栓塞大脑中动脉2 h后恢复灌注制备大鼠局灶性脑缺血再灌注模型，S组电针刺激百会穴旁2 mm处30 min，持续5 d，然后制备模型；E组电针刺激百会穴30 min，选取疏密波，强度1 mA，频率2/15 Hz，1次/d，连续5 d，然后制备模型。A组首先尾静脉注射miR-153激活剂50 μg/kg，其他处理同E组。C组不做任何处理。分别于再灌注24和48 h时行神经行为学评分，随后处死大鼠取海马组织，HE染色后观察海马CA1区病理学结果，采用Western blot和RT-PCR法分别检测海马核蛋白Nrf2、血红素加氧酶-1(HO-1)、醌氧化还原酶1(NQO-1)及其mRNA的表达，采用RT-PCR法检测海马miR-153的表达。n 结果:与C组相比，I/R组、S组、E组和A组神经行为学评分升高，再灌注各时点海马核蛋白Nrf2、HO-1、NQO1及其mRNA表达下调，miR-153表达上调(n P<0.05)；与I/R组和S组相比，E组和A组神经行为学评分降低，E组再灌注各时点海马核蛋白Nrf2、HO-1、NQO1及其mRNA表达上调，miR-153表达下调，A组再灌注各时点海马核蛋白Nrf2、HO-1和NQO1及其mRNA表达下调，miR-153表达上调(n P<0.05)；与E组相比，A组神经行为学评分升高，再灌注各时点海马核蛋白Nrf2及HO-1、NQO1及其mRNA表达下调，miR-153表达上调(n P<0.05)。A组海马病理学损伤程度较E组加重。n 结论:海马miR-153参与了电针预处理减轻大鼠脑缺血再灌注损伤的过程，与激活Nrf2/HO-1信号通路有关。“,”Objective:To evaluate the role of hippocampal mir-153 in reduction of cerebral ischemia-reperfusion (I/R) injury by electroacupuncture (EA) preconditioning in rats.Methods:A total of 150 clean-grade healthy male Sprague-Dawley rats, aged 8-12 weeks, weighing 200-250 g, were divided into 5 groups (n n=30 each) using a random number table method: control group (group C), cerebral I/R group (group I/R), sham EA group (group S), EA at baihui acupoint preconditioning group (group E), and miR-153 activator group (group A). In group I/R, focal cerebral I/R was produced by middle cerebral artery occlusion (MCAO) using a nylon thread with a rounded tip inserted into internal carotid artery and advanced cranially until resistance was met.MCAO was maintained for 2 h followed by reperfusion.The points 2 cm lateral to the acupoint Baihui were stimulated for 30 min for 5 consecutive days, and then the model was established in group S. The acupoint Baihui was stimulated with disperse-dense waves (1 mA, 2/15 Hz) for 30 min once a day for 5 consecutive days, and then the model was established in group E. In group A, mir-153 activator 50 μg/kg was injected via the tail vein, and the other treatments were similar to those previously described in group E. Group C did not receive any treatment.Neurobehavioral scores were assessed and recorded at 24 and 48 h of reperfusion, and then the rats were sacrificed, and hippocampal tissues were removed for examination of the pathological changes of hippocampal CA1 area after HE staining and for determination of the expression of heme oxygenase-1 (HO-1), quinone oxidoreductase 1 (NQO-1) protein and mRNA (by Western blot or real-time polymerase chain reaction) and expression of miR-153 (by real-time polymerase chain reaction).n Results:Compared with group C, neurobehavioral scores were significantly increased, and the expression of hippocampal nuclear proteins Nrf2, HO-1, NQO1 protein and mRNA was down-regulated, and the expression of miR-153 was up-regulated in I/R, S, E and A groups (n P<0.05). Compared with group I/R or group S, the neurobehavioral score was significantly decreased in E and A groups, the expression of hippocampal nuclear proteins Nrf2, HO-1, NQO1 protein and mRNA was significantly up-regulated, and the expression of miR-153 was down-regulated at each time point of reperfusion in group E, and the expression of hippocampal nuclear proteins Nrf2, HO-1 and NQO1 protein and mRNA was significantly down-regulated, and the expression of miR-153 was up-regulated at each time point of reperfusion in group A (n P<0.05). Compared with group E, the neurobehavioral score was significantly increased, and the expression of hippocampal nuclear proteins Nrf2, HO-1 and NQO1 protein and mRNA was down-regulated, and the expression of miR-153 was up-regulated at each time point of reperfusion in group A (n P<0.05). The pathological changes of hippocampus were accentuated in group A when compared with group E.n Conclusion:Hippocampal miR-153 is involved in reduction of cerebral I/R injury by EA preconditioning, and which is related to activating the Nrf2/HO-1 signaling pathway in rats.