【摘要】 目的评价电针内关穴对体外循环(CPB)大鼠心肌细胞凋亡与相关蛋白Bax、Bcl-2表达的影响。方法成年雄性SD大鼠60只,6~8月龄,体重400~450 g。采用随机数字表法,将大鼠随机分为3组(n=20):假手术组(S组)、CPB组和电针内关穴组(EA组)。采用尾动脉插管灌注,右颈静脉插管引流建立CPB模型。S组行麻醉和穿刺但不行CPB;CPB组行CPB 1 h;EA组行CPB 1h且在CPB期间使用电针刺激双侧内关穴。CPB结束后2 h处死大鼠并取左心室心肌组织,TUNEL法检测心肌细胞凋亡情况,Western blot法检测Bax和Bcl-2蛋白表达水平。结果与S组比较,CPB组和EA组心肌细胞凋亡指数升高,Bax和Bcl-2蛋白表达上调,Bax/Bcl-2比值上升(P<0.05);与CPB组比较,EA组心肌细胞凋亡指数下降,Bax蛋白表达下调,Bcl-2蛋白表达上调,Bax/Bcl-2比值下降(P<0.05)。结论电针内关穴对CPB大鼠的心肌细胞有明显的保护作用,其机制可能与调节凋亡相关蛋白Bax和Bcl-2的表达从而抑制细胞凋亡有关。更多还原

【Abstract】 Objective To investigate the effects of electroacupuncture at Neiguan point on myocardial apoptosis and the expression of apoptosis- related protein Bax and Bcl- 2 in rats undergoing cardiopulmonary bypass( CPB).Methods Sixty adult male Sprague- Dawley rats,aged 6 ~ 8 months,weighing 400 ~ 450 g,were randomly divided into3 groups( n = 20 each) : Sham operation group( Group S),Group CPB and electroacupuncture at Neiguan point group( Group EA). Tail arteries and right jugular vein were cannulated for CPB. Rats in Group S were anaesthetized and cannulated without CPB; rats in Group CPB were subjected to CPB for 1 h; and rats in Group EA were subjected to CPB for 1h and electroacupuncture at Neiguan point during CPB. Those animals were sacrificed 2 hours after CPB. Myocardium specimens were obtained from left ventricle for determination of apoptosis by TUNEL method,and the protein expression of Bax and Bcl- 2 by Western blot. Results Compared with Group S,the apoptosis index of myocardial cells and ratio of Bax / Bcl- 2 were significantly increased in Group CPB and Group EA( P < 0. 05),with significant up- regulation of the expression of Bax and Bcl- 2( P < 0. 05). Compared with Group CPB,the apoptosis index of myocardial cells and ratio of Bax / Bcl- 2 were significantly reduced in Group EA( P < 0. 05),with significant down- regulation of Bax and up- regulation of Bcl- 2( P < 0. 05). Conclusion Electroacupuncture at Neiguan has protective effects on myocardial cells in rats undergoing CPB,the mechanism is closely related to inhibiting myocardial apoptosis by adjusting the expression of apoptosis- related protein Bax and Bcl- 2.更多还原