Shenmai Injection Alleviates Cardiomyocyte Apoptosis Induced by Doxorubicin

Abstract

Background: Shenmai Injection (SMI) is a patented Chinese medicine extract, has been widely used to treat myocardial damage caused by doxorubicin (DOX), but its underlying mechanisms remain elusive. The study aimed to explore the protective effect of SMI on myocardial injury caused by DOX in vivo.Methods: The male Sprague-Dawley (SD) rats received DOX (2mg/kg) tail vein injection every week for 4 weeks, with or without SMI and miR-30a agomir treatment for 2 weeks. The protective effect of SMI on myocardial injury caused by DOX has been determined by measuring rat body mass and general heart morphology, myocardial pathological changes, and serum markers. The myocardial pathological changes were observed by Van Gieson (VG) staining, the serum marker levels of myocardial injury were detected by ELISA, the myocardial cell apoptosis was observed by TUNEL assay and transmission electron microscope, and the expression of target protein was detected by Western Blot.Results: SMI treatment significantly reduced rat HMI and LVMI, reduced the levels of serum CK, LDH, cTnT, NT-proBNP, and also reduced the levels of serum sST2 and GDF-15, and reduced the expression of rat myocardial type I and type III collagen, which was effective reduce the fibrosis of myocardial collagen knot tissue and interstitial. The study further found that SMI can increase the expression of Bcl-2 protein, reduce the expression of Bax, Caspase-9, and Caspase-3 protein, and reduce the apoptotic index of cardiomyocytes. Conclusion: The potential mechanism of SMI on cardiomyocytes from apoptosis induced by the DOX may be attributed to the regulation of miR-30a/beclin 1.