激动乙醛脱氢酶2对抗离体大鼠心肌缺血/再灌注损伤导致心律失常和氧化应激作用

Effect of activation of ALDH2 against myocardial ischemia /reperfusion injury rat induced arrhythmias and oxidative stress injury

目的观察乙醛脱氢酶2激动剂乙醇在对抗离体大鼠心肌缺血/再灌注(I/R)损伤致心律失常和氧化应激中的作用。方法大鼠分为I/R组和乙醛脱氢酶2激动剂乙醇+I/R组。乙醇+I/R组大鼠给予2.5%乙醇日常饮用,1 w后乙醇调整至5%,持续至第8周。采用Langendorff大鼠离体灌流技术,结扎冠状动脉前降支(LAD)30 min,复灌120 min后复制出大鼠离体心脏I/R损伤模型,观察复灌期间心律失常的发生率,测定冠脉流出液中乳酸脱氢酶(LDH)含量。实验结束后测定心肌组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性及乙醛脱氢酶2(ALDH2)活性。结果与I/R组相比,乙醇+I/R组大鼠心律失常的发生率和复灌流出液中LDH释放降低(P<0.05,P<0.01);心肌组织SOD、ALDH2活性增加(P<0.05),MDA含量降低(P<0.05)。结论长期应用低浓度乙醇可明显降低心律失常的发生,对抗离体心脏I/R损伤所致的氧化应激而发挥保护作用。

Objective To observe the role of activation of aldehyde dehydrogenase 2( ALDH2) on myocardial ischemia/reperfusion( I/R) injury induced arrhythmias and oxidative stress injury in rat. Methods Rats were divided into I/R and ethanol + I/R groups. Daily consumption of 2. 5% ethanol was used in ethanol + I / R group after one week,then the concentration of ethanol was changed to 5% until 8 weeks. The rat hearts were subjected to 30 min regional ischemia( occlusion of left anterior descending artery) and 120 min reperfusion ex vivo. The levels of arrhythmia were recorded and lactate dehydrogenase( LDH) content in coronary flow was determined. SOD activity,MDA content and ALDH2 activity were evaluated. Results Compared with I / R group,the levels of ventricular arrhythmia,LDH release and the content of MDA was decreased( P < 0. 05,P < 0. 01),SOD activity and ALDH2 activity were increased in ethanol + I / R group( P < 0. 05). Conclusions Long-term application of ethanol at low concentration can significantly reduce the levels of arrhythmias and be against the isolated heart I / R injury induced by oxidative stress.