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目的 :研究赤土茯苓苷 (Smiglabrin,Smi)对大鼠心肌缺血的保护作用。 方法 :采用结扎冠脉造成大鼠心肌缺血的模型 ,测量大鼠心肌梗塞面积、心电图 (ECG) S- T段抬高幅度 ,测定心肌组织中 SOD、CPK、MDA和FFA的活性和含量。 结果 :结扎冠脉后 ,心肌中 SOD、CPK活性降低 ,MDA、FFA含量升高 ,心电图表现为 S- T段升高 ,预先给予大白鼠大剂量 Sm i10 0 m g/ kg和小剂量 Smi5 0 m g/ kg,连续 7d腹腔注射 ,能明显改善缺血心电图 ,显著缩小心肌梗塞面积 ,心肌组织中 SOD和 CPK活力提高 ,MDA和 FFA含量降低。 结论 :Smi可能通过提高心肌中 SOD和 CPK活力 ,抑制 MDA和 FFA的生成而对冠脉结扎所造成的心肌损伤具有保护作用
Objective: To study the protective effect of siroglarin (Smi) on myocardial ischemia in rats. METHODS: A rat model of myocardial ischemia induced by coronary artery ligation was used to measure the myocardial infarct size and the amplitude of S-T segment elevation in electrocardiogram (ECG). The activity and content of SOD, CPK, MDA and FFA were measured. Results: After coronary artery occlusion, the activities of SOD and CPK in myocardium were decreased, and the contents of MDA and FFA were increased. The electrocardiogram showed an increase of S-T segment. Large doses of Sm i10 0 mg/kg and small doses of Smi5 0 mg were pre-administered to rats. / kg, intraperitoneal injection of continuous 7d, can significantly improve the ischemic electrocardiogram, significantly reduce myocardial infarct size, myocardial tissue SOD and CPK activity increased, MDA and FFA content decreased. Conclusion :Smi may protect myocardial damage caused by coronary artery ligation by increasing the activity of SOD and CPK in myocardium and inhibiting the production of MDA and FFA.