ω-3鱼油脂肪乳对乌头碱诱发大鼠心律失常的影响

Effect of omega-3 fatty acid on the experimental arrhythmic rats induced by aconitine

目的探讨ω-3鱼油脂肪乳对乌头碱诱发大鼠心律失常的影响及相关机制。方法 50只雄性大鼠随机分为ω-3鱼油脂肪乳组和对照组,每组25只。实验前15 d,ω-3鱼油脂肪乳组大鼠隔日经尾静脉注射ω-3鱼油脂肪乳2 mL.kg-1;对照组注射等量的生理盐水。应用乌头碱诱发心律失常大鼠模型,观察记录2组大鼠室性期前收缩、室性心动过速出现的时间及心律失常评分,Western blot检测大鼠心肌组织缝隙连接蛋白43(CX43)的表达。结果ω-3鱼油脂肪乳组大鼠室性期前收缩和室性心动过速出现时间均显著长于对照组(P<0.05)。静脉注射乌头碱后1 min,2组大鼠心律失常评分比较差异无统计学意义(P>0.05);静脉注射乌头碱后3、5、7 min,ω-3鱼油脂肪乳组大鼠心律失常评分均低于对照组(P<0.05)。ω-3鱼油脂肪乳组大鼠心肌组织中CX43蛋白的表达高于对照组(P<0.05),但2组大鼠心肌组织中去磷酸化CX43蛋白表达比较差异无统计学意义(P>0.05)。结论ω-3鱼油脂肪乳可能通过促进CX43的磷酸化改善乌头碱诱导的大鼠心律失常。

Objective To explore the effect and correlated mechanism of omega-3 （ω-3） fatty acid on the experimental arrhythmic rats induced by aconitine. Methods Fifty male rats were randomly divided into ω-3 fatty acids group and control group, twenty-five rats in each group. The rats in ω-3 fatty acids group were treated with 2 mL · kg- 1 ω-3 fatty acid by vena caudalis injection every other day for fifteen days ,while saline was injected in control group. Arrhythmic rats models were induced by aconitine. The emergence time of ventricular premature beat and ventricular fibrillation and the arrhythmic score were observed and recorded. The connexin-43 （ CX43 ） was detected by Western blot. Results The emergence time of ventricular premature beat and ventricular fibrillation in ω-3 fatty acids group was significantly longer than that in control group （P 〈 0. 05 ）. One minute after intravenous injection of aconitine, there was no statistical significance in the score of arrhythmia between two groups （P 〉 0.05 ）, while 3,5,7 minutes after intravenous injection of aconitine, the scores of arrhythmia in ω-3 fatty acids group were lower than these in control group（ P 〈0.05 ）. The expression of CX43 in myoeard tissues of rats in ω-3 fatty acids group was higher than that in control group （ P 〈 0.05 ） , however, there was no statistical significance in the expression of NP-CX43 between two groups（ P 〉 0.05 ）. Conclusion ω-3 fatty acids may improve aconitine-induced arrhythmia in rats by promoting the phosphorylation of CX43.