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目的研究玉郎伞黄酮类化合物(YLSF)对大鼠离体心脏缺血再灌注损伤的作用及其作用机制。方法采用Langen-dorff法灌流离体大鼠心脏,停灌30min后再灌30min,造成心肌缺血-再灌注损伤模型。于大鼠左心室插入水囊导管,记录YLSF对血流动力学指标的影响,测定冠脉流量(CF)和冠脉流出液中肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、乳酸脱氢酶同工酶-1(LDH-1)的活性及心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)的含量。结果 YLSF高剂量可显著改善缺血-再灌注所致大鼠的心功能损伤,减少CK、CK-MB、LDH、LDH-1的释放和MDA的产生,增加SOD的活性。结论 YLSF对心肌缺血-再灌注损伤具有保护作用,其机制可能与清除氧自由基、减少脂质过氧化反应有关。
Objective To investigate the effect and mechanism of YLSF on isolated rat hearts with ischemia-reperfusion injury. Methods The isolated rat heart was perfused with Langen-dorff method, then reperfusion 30 min after reperfusion for 30 min, resulting in myocardial ischemia-reperfusion injury model. The left ventricle was inserted into the balloon catheter to record the influence of YLSF on the hemodynamic parameters. The coronary flow (CF) MB), lactate dehydrogenase (LDH), lactate dehydrogenase isoenzyme-1 (LDH-1) and the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardium. Results High doses of YLSF could significantly improve the cardiac function, reduce the release of CK, CK-MB, LDH, LDH-1 and the production of MDA and increase the activity of SOD in ischemia-reperfusion-induced rats. Conclusion YLSF has a protective effect on myocardial ischemia-reperfusion injury, and its mechanism may be related to scavenging oxygen free radicals and reducing lipid peroxidation.