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目的 :通过大鼠离体心脏 L angendoff灌流 ,观察油茶皂苷 (sasanquqsaponin,SQS)对缺氧复氧 (anoxia/reoxygenation,A/ R)损伤的保护作用及其机制。方法 :A/ R为缺氧 40 m in再给氧 30 min;SQS0 .5 mg/ L 或Gliberclam ide30 μmol/ L + SQS0 .5 mg/ L 于缺氧复氧前 15 min灌流 15 m in,分别记录心功能及测量酶活性。结果 :与 A/ R组相比 ,SQS组能增加心肌的收缩功能 ,使氧自由基清除剂超氧化物歧化酶 (SOD) ,谷胱苷肽转移酶(GSH- Px)活性增强 ,脂质过氧化产物丙二醛 (MDA )生成减少 ,降低心肌组织钙含量 ,使肌酸激酶 (CK )生成减少 ,所以 SQS对心肌 A/ R损伤具有保护作用。在加入 KATP通道阻断剂 Gliberclam ide与 SQS同时灌注时 ,发现 SQS的上述作用消失。结论 :SQS的心肌保护与 KATP通道的开放有关。
OBJECTIVE : To investigate the protective effect of sasan quqsaponin (SQS) on anoxia/reoxygenation (A/R) injury and its mechanism by perfusion of isolated rat heart L angendoff. Methods: A / R was 40 min in hypoxia and 30 min in oxygen supplement; SQS 0.5 mg / L or Gliberclam ide 30 μmol / L + SQS 0.5 mg / L perfused 15 min in 15 min before hypoxia and reoxygenation. Record heart function and measure enzyme activity. RESULTS: Compared with the A/R group, the SQS group was able to increase the contractile function of the myocardium, making the oxygen radical scavenger superoxide dismutase (SOD), and the activity of the GSH-Px increased. Peroxidation product malondialdehyde (MDA) production decreased, reducing myocardial calcium content, so that creatine kinase (CK) generation decreased, so SQS has a protective effect on myocardial A / R injury. When the KATP channel blocker Gliberclam ide was added simultaneously with SQS, the above effects of SQS disappeared. Conclusion: The myocardial protection of SQS is related to the opening of KATP channels.