Naringin ameliorates mitochondrial lipid peroxides, antioxidants and lipids in isoproterenol-induced myocardial infarction in Wistar rats.

The present study was undertaken to evaluate the preventive role of naringin on mitochondrial lipid peroxides, antioxidants and lipids in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85 mg/kg) at an interval of 24 h for 2 days resulted in a significant increase in the levels of mitochondrial lipid peroxides with a significant decrease in the activities/levels of mitochondrial antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and reduced glutathione). ISO-induction also showed a significant increase in the levels of mitochondrial cholesterol, triglycerides and free fatty acids with a subsequent decrease in the levels of phospholipids. Oral pretreatment with naringin (10, 20 and 40 mg/kg) to ISO-induced rats daily for a period of 56 days significantly decreased the levels of mitochondrial lipid peroxides with a significant increase in the activities/levels of mitochondrial antioxidants and significantly minimized the alterations in the mitochondrial lipid levels in ISO-induced rats. Thus, the findings demonstrate that naringin prevents alterations in mitochondrial lipid peroxides, antioxidants and lipids in ISO-induced MI in rats.

Preventive effect of naringin on cardiac markers, electrocardiographic patterns and lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats.

Diets rich in natural antioxidants are associated with reduced risk of heart diseases. This study was aimed to evaluate the preventive role of naringin on cardiac troponin T (cTnT), lactate dehydrogenase (LDH)-isoenzyme, cardiac marker enzymes, electrocardiographic (ECG)-patterns and lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85mg/kg) at an interval of 24h for 2 days showed a significant increase in the levels of cTnT, intensity of the bands of LDH-isoenzyme (LDH1 and LDH2) and the activities of cardiac marker enzymes such as creatine kinase-MB (CK-MB), creatine kinase (CK), LDH, aspartate transaminase (AST) and alanine transaminase (ALT) in serum with subsequent decrease in the activities of CK, LDH, AST and ALT in the heart and alterations in ECG-patterns. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of beta-glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with naringin (10, 20 or 40mg/kg) daily for a period of 56 days positively altered the levels of cTnT, intensity of the bands of the LDH1 and LDH2-isoenzyme and the activities of cardiac marker enzymes, ECG-patterns and lysosomal hydrolases in ISO-induced rats. Thus, naringin possess cardioprotective effect in ISO-induced MI in rats.

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

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.

Preventive effect of naringin on lipid peroxides and antioxidants in isoproterenol-induced cardiotoxicity in Wistar rats: biochemical and histopathological evidences.

This study was designed to evaluate the cardioprotective potential of naringin on lipid peroxides, enzymatic and nonenzymatic antioxidants and histopathological findings in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (85 mg/kg) to male Wistar rats showed a significant increase in the levels of thiobarbituric acid reactive substances and lipid hydroperoxides in plasma and the heart and a significant decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase in the heart and the levels of reduced glutathione, vitamin C and vitamin E in plasma and heart and ceruloplasmin in plasma. Oral administration of naringin (10, 20 and 40 mg/kg, respectively) to ISO-induced rats daily for a period of 56 days showed a significant decrease in the levels of lipid peroxidative products and improved the antioxidant status by increasing the activities of antioxidant enzymes and nonenzymatic antioxidants. Histopathological findings of the myocardial tissue showed the protective role of naringin in ISO-induced rats. The effect at a dose of 40 mg/kg of naringin was more pronounced than that of the other two doses, 10 and 20mg/kg. The results of our study show that naringin possess anti-lipoperoxidative and antioxidant activity in experimentally induced cardiac toxicity.

Preventive effect of Aegle marmelos leaf extract on isoprenaline-induced myocardial infarction in rats: biochemical evidence.

We have evaluated the preventive effects of an aqueous Aegle marmelos leaf extract (AMLEt) in isoprenaline (isoproterenol)-induced myocardial infarction in rats. Rats were pretreated with AMLEt (50, 100 or 200 mg kg(-1)) for 35 days. After the treatment period, isoprenaline (200 mg kg(-1)) was administered subcutaneously to rats at an interval of 24 h for two days. The activity of creatine kinase (CK) and lactate dehydrogenase (LDH) was significantly increased in serum and significantly decreased in heart of isoprenaline-treated rats. Pretreatment with AMLEt decreased the activity of CK and LDH in serum and increased them in the heart. The activity of sodium-potassium dependent adenosine triphosphatase (Na(+)K(+)ATPase) was significantly decreased while the activity of calcium dependent adenosine triphosphatase (Ca(2+)ATPase) was simultaneously increased in the heart and aorta. AMLEt pretreatment increased the activity of Na(+)K(+) ATPase and decreased the activity of Ca(2+)ATPase in the heart and aorta simultaneously. The levels of cholesterol and triglycerides increased, while the levels of phospholipids decreased in the heart and aorta of isoprenaline-treated rats. In AMLEt-pretreated rats the levels of cholesterol and triglycerides decreased whereas phospholipids increased in heart and aorta. All the deranged biochemical parameters were restored with 200 mg kg(-1) AMLEt. Similarly alpha-tocopherol (60 mg kg(-1))-pretreatment to isoprenaline-treated rats exhibited a significant effect on all the parameters studied. The results from this study may have clinical relevance.

Comparative effects of Aegle marmelos extract and alpha-tocopherol on serum lipids, lipid peroxides and cardiac enzyme levels in rats with isoproterenol-induced myocardial infarction.

INTRODUCTION: We demonstrate the effect of Aegle marmelos leaf extract (AMLEt) and alpha-tocopherol on plasma lipids, lipid peroxides and marker enzymes in rats with isoproterenol (ISO)-induced myocardial infarction. METHODS: Rats were pre-treated orally for 35 days with different doses of an aqueous AMLEt (50 mg/ kg, 100 mg/kg and 200 mg/kg) prior to ISO-induced myocardial infarction. The effects on creatine kinase, lactate dehydrogenase, plasma thiobarbituric acid reactive substances, lipid hydroperoxides, serum lipids and lipoproteins were studied. RESULTS: Pre-treatment with AMLEt at doses of 100 mg/kg and 200 mg/kg bodyweight for 35 days showed a significant effect on the activities of marker enzymes, lipid peroxides, lipids, lipoproteins and antioxidant enzymes in ISO-treated rats. The effect of AMLEt 200 mg/kg was found to be equal to the effect of alpha-tocopherol 60 mg/kg. CONCLUSION: Aegle marmelos leaves possess antihyperlipidaemic effect in rats with ISO-induced myocardial infarction.

Effect of Aegle marmelos fruits on normal and streptozotocin-diabetic Wistar rats.

The present study evaluates the antidiabetic effect of an aqueous extract of Aegle marmelos fruits (AMFEt) in diabetes. Female albino Wistar rats were randomly divided into five groups: normal (untreated), normal + AMFEt, streptozotocin (STZ)-treated, STZ-treated + AMFEt, and STZ-treated + glibenclamide. Rats were rendered diabetic by STZ (45 mg/kg) administered intraperitoneally. AMFEt (250 mg/kg) was given twice daily for 1 month. Blood glucose, plasma insulin, glycosylated hemoglobin, liver glycogen, and change in body weight were determined. Food intake and water intake were monitored daily. An oral glucose tolerance test was also performed to determine the effect of this extract. The results show that glucose level and glycosylated hemoglobin were increased and plasma insulin and liver glycogen were decreased in diabetic rats, and that treatment with AMFEt reversed the effects of diabetes on these biochemical parameters to near-normal levels.

Preventive effect of naringin on cardiac mitochondrial enzymes during isoproterenol-induced myocardial infarction in rats: a transmission electron microscopic study.

Dietary flavonoids intake has been reported inversely related to the incidence of cardiovascular diseases (CVD). The present study is undertaken to evaluate the preventive role of naringin on mitochondrial enzymes in isoproterenol (ISO)-induced myocardial infarction in male albino Wistar rats. Rats subcutaneously injected with ISO (85 mg/kg) at an interval of 24 h for 2 days, resulting in significant (p < 0.05) increase in the levels of mitochondrial lipid peroxides. ISO-induction also showed significant (p < 0.05) decrease in the activities of mitochondrial tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, and alpha-ketoglutarate dehydrogenase) and respiratory chain enzymes (NADH dehydrogenase and cytochrome c oxidase). Oral pretreatment with naringin (10, 20, and 40 mg/kg) to ISO-induced rats daily for a period of 56 days significantly (p < 0.05) minimized the alterations in all the biochemical parameters and restored the normal mitochondrial function. Transmission electron microscopic (TEM) observations also correlated with these biochemical findings. Thus, our findings demonstrate that naringin prevents the mitochondrial dysfunction during ISO-induced myocardial infarction in rats.

Preventive effect of naringin on lipids, lipoproteins and lipid metabolic enzymes in isoproterenol-induced myocardial infarction in Wistar rats.

This study was designed to evaluate the preventive effect of naringin in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Rats were pretreated with naringin (10, 20, and 40 mg/kg body weight) orally for a period of 56 days. After the treatment period, ISO (85 mg/kg body weight) was administered subcutaneously to rats at an interval of 24 h for 2 days. There was a significant increase in the levels of total, ester, and free cholesterol, triglycerides (TG), and free fatty acids (FFA) in serum and heart and decrease in heart phospholipids (PL) in ISO-induced rats. Altered levels of lipoproteins and activities of 3-hydroxy-3-methylglutaryl-Coenzyme reductase A in liver and heart, lecithin cholesterol acyl transferase and lipoprotein lipase in plasma were also observed in ISO-induced rats. Pretreatment with naringin (10, 20, and 40 mg/kg) for a period of 56 days significantly decreased the levels of total, ester, and free cholesterol, TG, FFA in serum and heart and increased PL in heart. It also minimized the alterations in serum lipoproteins and lipid metabolic enzymes in ISO-induced rats. Thus, naringin has a lipid-lowering effect in ISO-induced MI rats.