Levosimendan can effectively reduce myocardial cell apoptosis caused by hypoxia through antioxidant activity

Abstract Levosimendan (LMSD) is a novel positive inotropic drug with unique chemical structure and pharmacological properties. It has multiple effects such as dilating blood vessels and improving myocardial diastolic function, and is widely used in the treatment of cardiovascular diseases such as acute heart failure in clinical practice. During clinical treatment, LMSD seems to have a certain protective effect on hypoxic myocardial cells. Therefore, the aim of this study is to determine the effect of LMSD on hypoxic cardiomyocytes, and to explore its mechanism of action on hypoxic cardiomyocytes, in order to promote its more rational use in clinical treatment. In this study, it was demonstrated through antioxidant experiments that LMSD has certain antioxidant capacity. In addition, adding LMSD to hypoxic cardiomyocytes can effectively reduce intracellular ROS levels and improve mitochondrial membrane potential changes caused by hypoxia. And reduce the Bax/Bcl-2 ratio, thereby reducing the apoptosis of myocardial cells under hypoxic conditions. The decrease in protein and mRNA expression levels of apoptotic protease activating factor‑1 (APAF-1) and Caspase-3 (CASP-3) in hypoxic cardiomyocytes demonstrates that LMSD effectively reduces apoptosis of hypoxic cardiomyocytes. Therefore, this study demonstrates that LMSD may reduce cell apoptosis by inhibiting mitochondrial damage under hypoxic conditions, and reveals the possible mechanism of LMSD's cardioprotective effect.