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目的:评价电针预处理减轻体外循环大鼠急性肺损伤的机制与胆碱能受体/高迁移率族蛋白B1(HMGB1)的关系。方法:SPF级健康雄性SD大鼠36只，3月龄，体重400～450 g，采用随机数字表法将大鼠分为3组(n n＝12)：假手术组(Sham组)、体外循环组(CPB组)和电针预处理组(EA组)。电针预处理：选择双侧足三里及肺俞穴，频率2/15 Hz，电流1～2 mA，强度以引起后肢轻微跳动为准，每次30 min，每日1次，连续治疗5 d。于末次电针结束后24 h时建立体外循环模型。体外循环结束后2 h时，取肺组织，采用Western blot法检测α7nAChR、M1受体以及HMGB1表达水平，HE染色观察病理学结果。n 结果:与Sham组相比，CPB组肺组织α7nAChR表达下调，M1受体和HMGB1表达上调(n P<0.05)；与CPB组相比，EA组肺组织α7nAChR表达上调，M1受体和HMGB1表达下调(n P<0.05)，肺组织病理学损伤减轻。n 结论:电针预处理减轻体外循环诱发大鼠急性肺损伤的机制可能与改善胆碱能受体失衡状态，降低HMGB1表达水平有关。“,”Objective:To evaluate the relationship between the mechanism of electroacupuncture (EA) preconditioning-induced acute lung injury and cholinergic receptor and high mobility group protein B1 (HMGB1) in the rats undergoing cardiopulmonary bypass (CPB).Methods:Thirty-six SPF healthy male Sprague-Dawley rats, aged 3 months, weighing 400-450 g, were divided into 3 groups (n n=12 each) by using a random number table method: sham operation group (group Sham), CPB group and EA preconditioning group (group EA). EA preconditioning was performed as follows: EA of bilateral Zusanli and Feishu acupoints (frequency 2/15 Hz, intensity 1-2 mA) lasting 30 min was performed once a day for 5 consecutive days.The model of CPB was established at 24 h after the last EA.At 2 h after the end of CPB, lung tissues were taken for determination of the expression of α7nAChR, M1 receptor and HMGB1 (by Western blot) and for examination of the pathological changes (by HE staining).n Results:Compared with group Sham, the expression of α7nAChR was significantly down-regulated, and the expression of M1 receptor and HMGB1 was up-regulated in group CPB ( n P<0.05). Compared with group CPB, the expression of α7nAChR was significantly up-regulated, the expression of M1 receptor and HMGB1 was down-regulated (n P<0.05), and the pathological changes of lung tissues were significantly attenuated in group EA.n Conclusion:The mechanism by which EA preconditioning reduces acute lung injury induced by CPB may be related to improving cholinergic receptor imbalance and decreasing HMGB1 expression in the rats.