Preventive effect of naringin on isoproterenol-induced cardiotoxicity in Wistar rats: an in vivo and in vitro study

Abstract

This study was aimed to evaluate the preventive role of naringin on heart weight, blood glucose, total proteins, albumin/globulin (A/G) ratio, serum uric acid, serum iron, plasma iron binding capacity and membrane bound enzymes such as sodium potassium-dependent adenosine triphosphatase (Na +/K + ATPase), calcium-dependent adenosine triphosphatase (Ca 2+ ATPase) and magnesium-dependent adenosine triphosphatase (Mg 2+ ATPase) and glycoproteins such as hexose, hexosamine, fucose and sialic acid in isoproterenol (ISO)-induced myocardial infarction (MI) in rats and in vitro free radical scavenging assay. Male albino Wistar rats were pretreated with naringin (10, 20 and 40 mg/kg, respectively) for a period of 56 days. After the treatment period, ISO (85 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days. ISO-induced rats showed a significant ( P < 0.05) increase in the heart weight, blood glucose, serum uric acid, serum iron and a significant ( P < 0.05) decrease in the levels of total proteins, A/G ratio and iron binding capacity. A significant ( P < 0.05) decrease in the activity of Na +/K + ATPase and increase in the activities of Ca 2+ and Mg 2+ ATPase in the heart and a significant ( P < 0.05) increase in the levels of glycoproteins in serum and the heart were also observed in ISO-induced rats. Pretreatment with naringin for a period of 56 days exhibited a significant ( P < 0.05) effect and altered these biochemical parameters positively in ISO-induced rats. Naringin also scavenges 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2′-azinobis-(3-ethyl-benzothiazoline-6-sulfonic acid) (ABTS) and nitric oxide (NO) radicals in vitro. Thus, our study shows that naringin has cardioprotective role in ISO-induced MI in rats.