摘要
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。
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 for 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 for 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 Ca 2+ accumulation These influences of SQS were attenuated by the K ATP channel blocker, Glibenclamide Thus SQS proved to play a protective action on myocardial ischemia induced by A/R, with the mechanism of action involving the opening of K ATP channel
出处
《中草药》
CAS
CSCD
北大核心
2000年第11期841-843,共3页
Chinese Traditional and Herbal Drugs
基金
江西省自然科学基金资助项目。
