Abstract
Background Levosimendan preconditioning has been shown to attenuate myocardial apoptosis in animal models. However, protective effects of levosimendan postconditioning against myocardial apoptosis following myocardial infarction (MI) have not been evaluated. Therefore, we investigated the effects of levosimendan postconditioning on myocardial apoptosis in MI rat models. Methods In an anoxia/reoxygenation (A/R) model, H9c2 cells were pretreated with or without levosimendan postconditioning after which their apoptosis rates were assessed by flow cytometry, RT-qPCR, and western blot analyses. Then, postconditioning was performed with or without levosimendan in MI rat models. Myocardiocyte apoptosis was evaluated by echocardiography, TTC staining, TUNEL staining, immunohistochemical staining, RT-qPCR, and western blot analysis. Results Levosimendan postconditioning inhibited H9c2 cell apoptosis in A/R models by elevating Bcl-2 while suppressing Caspase-3 and Bax at both mRNA and protein levels. Moreover, it improved cardiac functions and reduced the left ventricle infarction area in MI rat models. Compared to the MI control group, cardiomyocyte apoptosis rates in the levosimendan postconditioning group were low. The reduced cardiomyocyte apoptosis rates were associated with downregulation of Bax and Caspase-3 as well as with upregulation of Bcl-2 at mRNA and protein levels. Conclusions Levosimendan postconditioning of MI rat models protected against cardiomyocyte apoptosis, implying that it is a potential strategy for preventing cardiomyocyte apoptosis in the treatment of cardiac dysfunction following MI.
Highlights
Acute or chronic myocardial infarction is caused by myocardial cell ischemia following coronary artery obstruction, resulting in secondary myocardial cell necrosis [1]
To elucidate on the therapeutic effects of levosimendan postconditioning following MI, we investigated its antiapoptotic effects in in vitro anoxia-reoxygenation (A/R) models. en, we established in vivo acute myocardial infarction (AMI) models to observe the effect of levosimendan on cardiomyocyte after MI. us, we will clarify a point to determine whether this treatment has protective effects against cardiomyocyte apoptosis following MI. is effect has a positive significance for clarifying the relevant mechanism of cardiomyocyte apoptosis
E H9c2 cells (Shanghai Institute for Biological Sciences) were cultured in the anoxic media for 3 h and centrifuged. en, anoxic H9c2 cells were placed in reoxygenation media for 2 h after which the cell suspension was centrifuged to obtain the cells. e anoxic/reoxygenated H9c2 cells were divided into two groups: A/R and the A/ R + levosimendan (A/R + Levo) groups
Summary
Acute or chronic myocardial infarction is caused by myocardial cell ischemia following coronary artery obstruction, resulting in secondary myocardial cell necrosis [1]. Erefore, the diagnosis of MI, device and drug treatment, and prevention as well as mechanism research on how to improve the function of cardiomyocyte are becoming the focus of research It is a great significance for improving the heart function and survival rate of patients with MI [1, 4]. Levosimendan postconditioning inhibited H9c2 cell apoptosis in A/R models by elevating Bcl-2 while suppressing Caspase-3 and Bax at both mRNA and protein levels. It improved cardiac functions and reduced the left ventricle infarction area in MI rat models. Levosimendan postconditioning of MI rat models protected against cardiomyocyte apoptosis, implying that it is a potential strategy for preventing cardiomyocyte apoptosis in the treatment of cardiac dysfunction following MI
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