摘要
目的探讨左旋卡尼汀在心肌缺血/再灌注(MI/R)损伤状态下对心肌的抗氧化作用及其可能机制。方法制备兔缺血/再灌注(MI/R)模型,缺血30min,分别再灌注1h、3h、5h的健康新西兰大白兔35只,对照组(1组,n=5)用丝线穿过冠状动脉左心室支但不结扎;MI/R组(2组,n=15;再均分为3个亚组)MI后分别静脉滴注生理盐水至实验结束;左旋卡尼汀治疗组(3组,n=15;再均分为3个亚组),MI后将左旋卡尼汀3.0g加入生理盐水250mL静脉滴注至实验结束。观察指标:1)缺血/再灌注过程中心电图的动态改变;2)再灌注结束后,动脉血游离脂肪酸(FFA)含量及组织中Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性;3)用Westernblot法检测结扎点以下5mm处左右心室全层心肌热休克蛋白70(HSP70)含量。结果1)2组和3组均出现明显的心电图动态改变,与2组比较,3组心电图ST段出现有效改善;2)在对应的时间点3组与2组相比,FFA含量显著减少(P<0.05),Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性明显增高;HSP70含量显著增多(P<0.05)。结论左旋卡尼汀对心肌缺血/再灌注损伤有确切的保护作用。利用游离脂肪酸进行β-氧化,优化能量代谢,可能是左旋卡尼汀保护心肌的机制之一;左旋卡尼汀可能是通过诱导热休克蛋白发挥抗氧化作用。
Objective To study the antioxidation effects of L-carnitine against ischemia/reperfusion injury of rabbit eardiomyoeytes in vivo and its possible mechanism. Methods Myocardial ischemia/reperfusion models were built in healthy New Zealand rabbits. Rabbits were subjected to 30 min myocardial ischemia followed by reperfusion for 1 h, 3 h, 5 h. Anesthetized rabbits were randomly divided into 3 groups： control group（ n = 5 ） in which left anterior descending coronary artery was exposed and a piece of silk thread was placed around the artery but not tied; MI/R group（n = 15, then equally subgroup） in which normal saline was infused into subllngual vein after MI; L-carnitine group（ n = 15, then equally subgroup） received intravenous L-carnitine 3.0 g and saline 250 mL after MI. ECG monitoring throughout the experiment, free fatty acid（ FFA）, myocardial Na^＋-K^＋--ATPase and Ca^2＋ -Mg^2＋ -ATPase were all observed after reperfusion. The content of heat shock protein 70 （ HSP 70 ） obtained 5 mm below the ischemia/ reperfusion region throughout the myocardial layer was determined with Western blot. Results MI/R caused significant changes in ECG and FFA compared with the control groups. The L-carnitine group showed protection against MI/R injury as evidenced by more effective improvement in ST of ECG, marked increase in Na^＋-K ^＋-ATPase and Ca^2＋ -Mg^2＋ -ATPase and marked decrease in FFA （ P 〈 0.05 ）. The content of HSP 70 was also dramatically increased. Conclusion L-carnitine can protect cardiomyocyte from ischemia/reperfusion injury; β-oxidation with free fatty acid improves energy metablism, stabilizes cell membrane probably by inducing HSP70 which will produce antioxidation function to protect myocardial cells.
出处
《首都医科大学学报》
CAS
2008年第1期78-80,共3页
Journal of Capital Medical University
