Study On The Cardiac Function Of Schisandrin B In Myocardial Infarction Mice

Objective:Create mice model of myocardial infarction to lay a foundation for the study of mechanisms of myocardial infarction by drug treatment.Methods:After fasting and no drinking for4hours, C57BL/6J mice were intraperitoneally anesthetized with pentobarbital sodium. Then mice were placed on a heating pad to maintain normothermia and then fixed in the supine position by tying the legs and the upper jaw. Then they were intubated, and ventilated to perform a left thoracotomy to expose the heart. The electrocardiogram, heart rate and respiratory rate were continuously monitored. Myocardial infarction was induced by permanent ligation of the left anterior descending coronary artery, using an8-0polypropylene suture passed about2-3mm from the inferior margin of left auricle. Ischemia was confirmed by myocardial blanching and ECG ST-segment elevation.Results:All C57BL/6J mice were successfully induced to myocardial infarction model. Three week after the operation, through the echocardiography measurement of left ventricular ejection fraction and other indexes, all C57BL/6J mice developed myocardial remodeling and some of them eventually died.Conclusion:Ligation of coronary artery is a simple, reliable and practicable method to induce myocardial infarction. And its achievement ratio is high. The mouse model of myocardial infarction is a good way to study of mechanisms of ischemic heart disease by drug treatment. Objective:To investigate whether Schisandrin B (Sch B) could improve cardiac function and attenuate myocardial remodeling after myocardial infarction (MI) in mice.Methods:Mice model of MI was established by permanent ligation of the left anterior descending (LAD) coronary artery. Then the MI mice were randomly treated with Sch B (n=20) or vehicle alone (n=20). After treatment for3weeks, cardiac function was detected by echocardiography measurement. Infarction size was detected by Evans blue and TTC staining. H&E and Masson trichrome staining were used. TNF-α, TGF-β1, IL-1β were detected by ELISA. NF-κB, Bcl-2, Bax, eNOS, phosphorylated eNOS, GATA4were detected by Western Blot. And BrdU was detected by immunohistochemistry.Results:3weeks after operation, Sch B could increase survival rate, improve heart function and decrease infarct size compared with vehicle. Moreover, Sch B could down-regulate some inflammatory cytokines, activate eNOS pathway, inhibit cell apoptosis, and enhance cell proliferation. Further in vitro study on H9c2cells showed similar effects of Sch B on prevention of hypoxia induced inflammation and cell apoptosis.Conclusion:Our results demonstrate that Sch B can reducer inflammation, inhibit apoptosis, and improve cardiac function after ischemic injury. It represents a potential novel therapeutic approach for treatment of ischemic heart disease.