Abstract
The aim of the present study was to look into the possible protective effects of glycyrrhizic acid (GA) against isoproterenol-induced acute myocardial infarction in Sprague-Dawley rats. The effect of three doses of glycyrrhizic acid in response to isoproterenol (ISO)-induced changes in 8-isoprostane, lipid hydroperoxides, super oxide dismutase and total glutathione were evaluated. Male Sprague-Dawley rats were divided into control, ISO-control, glycyrrhizic acid alone (in three doses-5, 10 and 20 mg/kg BW) and ISO with glycyrrhizic acid (in three doses) groups. ISO was administered at 85 mg/kg BW at two consecutive days and glycyrrhizic acid was administered intraperitoneally for 14 days. There was a significant increase in 8-isoprostane (IP) and lipid hydroperoxide (LPO) level in ISO-control group. A significant decrease in total superoxide dismutase (SOD) and total glutathione (GSH) was seen with ISO-induced acute myocardial infarction. Treatment with GA significantly increased SOD and GSH levels and decreased myocardial LPO and IP levels. Histopathologically, severe myocardial necrosis and nuclear pyknosis and hypertrophy were seen in ISO-control group, which was significantly reduced with GA treatment. Gycyrrhizic acid treatment proved to be effective against isoproterenol-induced acute myocardial infarction in rats and GA acts as a powerful antioxidant and reduces the myocardial lipid hydroperoxide and 8-isoprostane level.
Highlights
Myocardial infarction (MI) occurs when there is myocardial necrosis due to prolonged imbalance between the myocardial oxygen supply and demand of the myocardium [1]
There was a significant difference in the body weight between control and ISO-control group (p < 0.05)
Higher dose of glycyrrhizic acid (GA) significantly reduced (p < 0.05) cardiac hypertrophy caused by isoproterenol treatment (Table 1)
Summary
Myocardial infarction (MI) occurs when there is myocardial necrosis due to prolonged imbalance between the myocardial oxygen supply and demand of the myocardium [1]. Myocardial infarction is said to be part of a spectrum of diseases known as Acute Coronary Syndromes (ACS). The diseases that make up the spectrum are unstable angina, acute myocardial infarction, and sudden cardiac death [2,3]. Isoproterenol is a beta-adrenoceptor agonist that induces myocardial infarction by causing imbalance between oxidants and antioxidants in the myocardium [5,6]. Several antioxidants have been tested for their possible protective actions against acute myocardial infarction [7,8]. Antioxidants suppress the formation of reactive oxygen species and shift the balance towards antioxidants from pro-oxidants, which accumulate to protect the myocytes [6,9]. A recent report by Lee et al [11] demonstrated that glycyrrhizic acid was able to attenuate oxidative damage induced by carbon tetrachloride induced hepatic damage in mice
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