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 min再给氧 30 min;SQS0 .5 mg/ L 或Gliberclamide 30μmol/ L + SQS 0.5 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 K_ATP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 K_ATP通道的开放有关。

The protective effect and mechanism of action of sasanquasaponin (SQS) on isolated rat myocardial anoxia/reoxygenation(A/R) injury were studied. Rat A/R models were prepared by allowing the isolated rat heart to be injured fo r 40 min at anoxic condition and then followed by 30 min reoxygenation. SQS 0.5 mg/L and Glibenclamide 30 μmol/L + SQS 0.5 mg/L were perfused for 15 min before A/R and lasted fo r 30 min. Cardiac muscle contractility and the activities of enzymes were examined. results of the study showed that SQS improved cardiac muscle contractility, caused a significiant reduction of lipid peroxidation product, malondialdehyde(MDA), increased the activity of myocardium superoxide dismutase(SOD), glutathione peroxidase(GSH-PX), decreased creatine kinase(CK) concentration in the coronary outflow, and attenuated myocardial cell Ca2+ accumulation. These influences of SQS were attenuated by the K_ATP channel blocker, Glibenclamide. Thus SQS proved to play aprotective action on myocardial ischemia induced by A/R, with the mechanism of action involving the opening o f K_ATP channel.

江西省自然科学基金