Maslinic acid ameliorate electrolytes, membrane bound ATPases, antioxidants and histopathology in isoprenaline attenuated myocardial toxicity in rats

Abstract

ObjectivesMaslinic acid (MA), a natural compound widely distributed in many fruits and vegetables exhibited vast biological properties. Myocardial infarction (MI) is the most common cause of cardiovascular diseases morbidity and mortality. In this study cardioprotection of MA against isoprenaline (ISO) induced biochemical and histopathological alterations have been evaluated. MethodsRats were pretreated with MA (15 mg/kg) for 7 days and MI was induced with administration of ISO (85 mg/kg) on 8th and 9th days. Gallic acid (15 mg/kg) was used as positive control. Blood and heart were collected on 10th day from sacrificed rats and subjected to biochemical and histopathological analysis. ResultsISO administration significantly increased the enzymes creatine kinase-MB, lactate dehydrogenase, and alkaline phosphatase in serum whereas significantly decreased the marker enzymes in heart homogenate. ISO administration significantly increased the electrolytes sodium and calcium whereas significantly decreased potassium in heart homogenate. ISO showed a significant decrease in membrane bound adenosine triphosphatase (ATPase) enzymes sodium/potassium, calcium and magnesium ATPase in heart homogenate. ISO also significantly decreased the antioxidants reduced glutathione, glutathione S-transferase and glutathione peroxidase in heart homogenate. Furthermore, pretreatment of MA and GA reduced the effect of ISO significantly on all parameters studied. Furthermore, the cardioprotection of MA was also supported by histopathology. ConclusionsThis is the first report revealed that MA attenuates ISO-induced cardiac toxicity by ameliorating biochemical parameters such as cardiac marker enzymes, electrolytes, membrane bound ATPases and increased the antioxidants. The possible cardioprotective mechanism is due to the stabilization of myocardial membrane and antioxidant activity of MA.