OBJECTIVE: The objective was to evaluate the protective effect of ellagic acid against experimentally induced cardiac arrhythmias, hypertrophy and its association with altered lipid metabolism during myocardial infarction in rats. METHODS: Rats were treated with ellagic acid (7.5 and 15 mg/kg) orally for a period of 10 days. After 10 days of pretreatment, isoproterenol (100 mg/kg) was injected subcutaneously at an interval of 24 h for 2 days to induce myocardial infarction. On the 12th day, the cardiac rhythm was observed. The rats were sacrificed and the heart was isolated from each rat. Ventricular hypertrophy and myocardial necrotic scores were analysed in the myocardium. Lipid peroxidation products in the plasma were analysed. Changes in the lipid profile were measured using the plasma and heart tissue homogenates of normal and experimental rats. RESULTS: Isoproterenol-induced rats showed arrhythmias, hypertrophy and increased levels of myoglobin, creatine kinase-MB, lipid peroxidation products compared to the normal control rats. Ventricular hypertrophy and increased myocardial necrotic scores were observed in isoproterenol-induced rats. Oral pretreatment with ellagic acid restored pathological arrhythmias, ventricular hypertrophy, lipid peroxidation, altered lipid profile and myocardial necrosis in the isoproterenol-induced myocardial infarcted rats. CONCLUSIONS: Oral pretreatment with ellagic acid was safe and effective in cardio protection against ISO-induced arrhythmias, hypertrophy and myocardial necrosis. Anti lipid peroxidation property and anti hyperlipidaemic activity through 3-hydroxy-3 methyl glutaryl CoA reductase inhibition by ellagic acid may be the reasons for the beneficial action of ellagic acid against experimentally induced myocardial infarction.
OBJECTIVE: The objective was to evaluate the protective effect of ellagic acid against experimentally induced cardiac arrhythmias, hypertrophy and its association with altered lipid metabolism during myocardial infarction in rats. METHODS:Rats were treated with ellagic acid (7.5 and 15 mg/kg) orally for a period of 10 days. After 10 days of pretreatment, isoproterenol (100 mg/kg) was injected subcutaneously at an interval of 24 h for 2 days to induce myocardial infarction. On the 12th day, the cardiac rhythm was observed. The rats were sacrificed and the heart was isolated from each rat. Ventricular hypertrophy and myocardial necrotic scores were analysed in the myocardium. Lipid peroxidation products in the plasma were analysed. Changes in the lipid profile were measured using the plasma and heart tissue homogenates of normal and experimental rats. RESULTS:Isoproterenol-induced rats showed arrhythmias, hypertrophy and increased levels of myoglobin, creatine kinase-MB, lipid peroxidation products compared to the normal control rats. Ventricular hypertrophy and increased myocardial necrotic scores were observed in isoproterenol-induced rats. Oral pretreatment with ellagic acid restored pathological arrhythmias, ventricular hypertrophy, lipid peroxidation, altered lipid profile and myocardial necrosis in the isoproterenol-induced myocardial infarctedrats. CONCLUSIONS: Oral pretreatment with ellagic acid was safe and effective in cardio protection against ISO-induced arrhythmias, hypertrophy and myocardial necrosis. Anti lipid peroxidation property and anti hyperlipidaemic activity through 3-hydroxy-3 methyl glutaryl CoA reductase inhibition by ellagic acid may be the reasons for the beneficial action of ellagic acid against experimentally induced myocardial infarction.