T89 and Its Components Ameliorate Oxidative Stress and Energy Metabolism Disorders in Rats with Myocardial Ischemia/Reperfusion Injury

Objective: Cardiotonic pills (T 89 ) promote blood circulation and remove blood stasis and are commonly used to treat coronary heart disease and angina pectoris in clinical practice. Our previous studies have demonstrated that T 89 alleviates ischemia/reperfusion (I/R)-induced myocardial injury in rats. However, the roles of its main active components, namely total salvianolic acids (TSA) and Panax notoginseng saponins (PNS), remain unclear. Therefore, this study aimed to investigate the protective effects of T 89 and its key components, TSA and PNS, on myocardial I/R injury. Materials and Methods: Male Sprague–Dawley rats were pretreated with T 89 or one of its main components. They underwent ligation of the left anterior descending coronary artery for 30 min, followed by 24 h of reperfusion. At 24 h after reperfusion, we assessed the myocardial infarction area, myocardial blood flow, cardiomyocyte apoptosis, myocardial structure, energy metabolism, mitochondrial complex activity, and the expression of related proteins. Results: Pretreatment with T 89 attenuated I/R-induced myocardial damage, including a reduced infarct size, lower levels of myocardial injury markers, reduced cardiomyocyte apoptosis, improved myocardial blood flow, and preservation of F-actin. Mechanistically, TSA increased sirtuin 1 (SIRT1) and NADH dehydrogenase (ubiquinone) 1 alpha subcomplex subunit 10 (NDUFA10) expression following I/R, thereby enhancing Complex I activity; meanwhile, PNS restored adenosine triphosphate (ATP) synthase activity and Complex IV activity, increased myocardial ATP content, and improved energy metabolism. Conclusions: Pretreatment with T 89 protects the myocardium from I/R injury. This protective effect may be mediated by the antioxidant activity of TSA and the enhancement of energy metabolism by PNS.