目的:探讨颈迷走神经刺激(CVNS)对大鼠心肌缺血再灌注(IR)损伤的影响及可能的机制.方法:24只,成年雄性,SPF级大鼠(200 ～ 250g),随机分为假手术组(sO,n＝8)、缺血再灌注组(n＝8)和颈迷走神经刺激+ I/R组(CVNS+ I/R,n =8).选用I/R模型(缺血30min,再灌注4h).假手术组仅开胸、穿线,但不结扎.再灌注2h后取颈静脉血和心肌组织,分别检测心肌损伤标志物:肌酸激酶(CK)和肌钙蛋白I (cTnI);氧化应激水平:丙二醛(MDA)水平和超氧化物歧化酶(SOD)活性;B细胞淋巴瘤/白血病2(Bcl-2)表达;细胞自噬水平:beclin-1和LC3-Ⅱ/Ⅰ表达.结果:与SO组比较,I/R组中CK、cTnI、MDA、Beclin-1和LC3-Ⅱ/Ⅰ显著增加(P＜0.05),SOD活性显著降低(P＜0.05),Bcl-2表达呈下降趋势,但差异无统计学意义(P＞0.05);与IR组比较,CVNS可以显著抑制CK、cTnI、MDA、Beclin-1和LC3-Ⅱ/Ⅰ的表达(P＜0.05),增加Bcl-2的表达和SOD的活性(P＜0.05).结论:CVNS可以显著抑制:①大鼠心肌IR损伤;②心肌细胞过度自噬,机制可能与增加Bcl-2表达、抑制氧化应激水平有关.%Objective:To investigate the effects of cervical vagus nerve stimulaiton (CVNS) on myocardial IR injury and possible mechanisms.Methods:Twenty four male rats were randomly divided into 3 groups:sham operate group (SO,n =8),IR group (n =8) and CVNS + IR group (n =8).IR model (ischemia 30 min and reperfusion 4h) were used.After 4h reperfusion,Jugular venous blood and myocardial tissue were collected for detecting.Myocardial injury marker:the serum lactate dehydrogenase (LDH) and creatine kinase (CK) level,oxidative stress:malonaldehyde (MDA) level and superoxide dismutase (SOD) activity;Bcl-2 expression and autophagy proteins:beclin-1 and LC3-Ⅱ/Ⅰ were detected.Results:compared with SO group,the expression of creatine kinase (CK),troponin Ⅰ (cTnI),MDA,beclin-1,LC3-Ⅱ/Ⅰ significantly increased (P ＜ 0.05),the activity of SOD decreased (P ＜ 0.05),the expression of Bcl-2 revealed a decreased trend (P ＞ 0.05) in IR group.Compared with IR group,CVNS could significantly decrease the expression of CK,cTnI,MDA,beclin-1 and LC3-Ⅱ/Ⅰ,significantly increase the expression of Bcl-2 and SOD activity (P ＜ 0.05).Conclusion:CVNS could effectively 1) suppress mycoardial IR injury and 2) autophagy over activation,which might associated with increased Bcl-2 level and decreased oxidative stress.
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