Abstract
Background Cardiovascular disease (CVD) is a group of heart disorders, which is a major cause of noncommunicable disease-related mortalities worldwide. Myocardial infarction (MI) is an acute disorder due to the poor supply of oxygen and blood to the myocardium. MI is the foremost form of CVD, which is the primary cause of mortality worldwide. Objectives Here, we intended to discover the ameliorative properties of the ponicidin against the isoproterenol (ISO)-stimulated MI in rats. Methodology About 85 mg/kg of ISO was administered to the rats to trigger the MI and then treated with 25 and 50 mg/kg of ponicidin. The body weight and heart weight of all rats were determined. The total protein, c-reactive protein (CRP), and uric acid levels were examined. The activities of cardiac function markers such as creatine kinase (CK), ALT, AST, and gamma-glutamyl transferase (GGT) were examined. The antioxidants such as glutathione (GSH), GST, and GPx were examined by the previous methods. The status of Na+/K+, Mg2+, and Ca2+ ATPase activities was assessed using kits. The status of Na+, K+, and Ca2+ ions and inflammatory makers such as TNF-alpha and IL-6 were investigated using respective kits. The histopathological analysis was performed on the heart tissues to detect the histological changes. Results The results revealed that ponicidin increased body weight and decreased heart weight in MI rats. The status of CRP and uric acid was decreased and total protein was augmented in the ponicidin-treated MI rats. The AST, ALT, CK, and GGT activities were appreciably decreased in serum and elevated in the cardiac tissues of the ponicidin-administered MI rats. Furthermore, the ponicidin improved the antioxidant levels, decreased the TNF-alpha and IL-6, and regulated the Na+, K+, and Ca2+ ion transports in the MI rats. The activities of Na+/K+, Mg2+, and Ca2+ ATPase enzymes were remarkably increased in the heart tissues by the ponicidin-treated MI rats. Ponicidin treatment also ameliorated the ISO-stimulated histological alterations in the heart tissue of the MI rats. Conclusion Ponicidin treatment appreciably improved the antioxidants, Na+/K+, Mg2+, and Ca2+ ATPase enzyme activities, decreased the inflammatory markers, and regulated the cardiac marker enzyme activities in the MI rats. Hence, it can be a talented therapeutic candidate in the future to treat MI.