Ellagic acid inhibits cardiac arrhythmias, hypertrophy and hyperlipidaemia during myocardial infarction in rats.

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.

Protective efficacy of ellagic acid on glycoproteins, hematological parameters, biochemical changes, and electrolytes in myocardial infarcted rats.

The cardioprotective property of ellagic acid in rats has been reported previously. The present study reveals the protective role of ellagic acid in biochemical parameters including serum iron, plasma iron binding capacity, uric acid, glycoprotein, and electrolytes along with hematological parameters. Rats were subcutaneously injected with isoproterenol (ISO) (100 mg/kg) for 2 days to induce myocardial infarction. ISO-induced rats showed a significant increase in their levels of serum iron, serum uric acid, and blood glucose, and a significant decrease in their levels of plasma iron binding capacity, serum total protein, albumin/globulin ratio, and heart glycogen, when compared with normal control rats. The altered hematological parameters were also observed in ISO-induced rats when compared with normal control rats. Pretreatment with ellagic acid at doses of 7.5 and 15 mg/kg produced significant beneficial effect by returning all the above-mentioned biochemical and hematological parameters to near normal levels.

Ellagic acid ameliorates isoproterenol induced oxidative stress: Evidence from electrocardiological, biochemical and histological study.

The present study was designed to evaluate the cardioprotective effects of ellagic acid against isoproterenol induced myocardial infarction in rats by studying electrocardiography, blood pressure, cardiac markers, lipid peroxidation, antioxidant defense system and histological changes. Male Wistar rats were treated orally with ellagic acid (7.5 and 15mg/kg) daily for a period of 10 days. After 10 days of pretreatment, isoproterenol (100mg/kg) was injected subcutaneously to rats at an interval of 24h for 2 days to induce myocardial infarction. Isoproterenol administered rats showed significant changes in the electrocardiogram pattern, arterial pressure, and heart rate. Isoproterenol-induced rats also showed significant (P<0.05) increase in the levels of serum troponin-I, creatine kinase, lactate dehydrogenase, C-reactive protein, plasma homocysteine, heart tissue thiobarbituric acid reactive substances and lipid hydro peroxides. The activities/levels of antioxidant system were decreased in isoproterenol-induced rats. The histopathological findings of the myocardial tissue evidenced myocardial damage in isoproterenol induced rats. The oral pretreatment of ellagic acid restored the pathological electrocardiographic patterns, regulated the arterial blood pressures and heart rate in the isoproterenol induced myocardial infarcted rats. The ellagic acid pretreatment significantly reduced the levels of biochemical markers, lipid peroxidation and significantly increased the activities/levels of the antioxidant system in the isoproterenol induced rats. An inhibited myocardial necrosis was evidenced by the histopathological findings in ellagic acid pretreated isoproterenol induced rats. Our study shows that oral pretreatment of ellagic acid prevents isoproterenol induced oxidative stress in myocardial infarction.