(-) Epicatechin prevents alterations in lysosomal glycohydrolases, cathepsins and reduces myocardial infarct size in isoproterenol-induced myocardial infarcted rats.

The preventive effects of (-) epicatechin on oxidative stress, cardiac mitochondrial damage, altered membrane bound adenosine triphosphatases and minerals were reported previously in isoproterenol-induced myocardial infarction model. Leakage of lysosomal glycohydrolases and cathepsins play an important role in the pathology of myocardial infarction. This study was aimed to evaluate the preventive effects of (-) epicatechin on alterations in lysosomal glycohydrolases, cathepsins and myocardial infarct size in isoproterenol-induced myocardial infarcted rats. Male albino Wistar rats were pretreated with (-) epicatechin (20mg/kg body weight) daily for a period of 21 days. After the pretreatment period, isoproterenol (100mg/kg body weight) was injected subcutaneously into the rats at an interval of 24h for two days to induce myocardial infarction. The levels of serum cardiac troponin-I and the activities of serum and heart lysosomal enzymes (ß-glucuronidase, ß-N-acetyl glucosaminidase, ß-galactosidase, cathepsin-B and cathepsin-D) were increased significantly (P<0.05) and the activities of ß-glucuronidase and cathepsin-D in the heart lysosomal fractions were significantly (P<0.05) decreased in isoproterenol-induced myocardial infarcted rats. The in vitro study revealed the potent antioxidant action of (-) epicatechin. Pretreatment with (-) epicatechin daily for a period of 21 days prevented the leakage of cardiac marker, lysosomal glycohydrolases, cathepsins, and reduced infarct size, thereby protecting the lysosomal membranes in isoproterenol-induced myocardial infarcted rats, by virtue of its membrane stabilizing property.

Protective effects of thymol on altered plasma lipid peroxidation and nonenzymic antioxidants in isoproterenol-induced myocardial infarcted rats.

This study evaluates the protective effects of thymol on altered plasma lipid peroxidation products and nonenzymic antioxidants in isoproterenol (ISO)-induced myocardial infarcted rats. Male albino Wistar rats were pre and cotreated with thymol (7.5 mg/kg body weight) daily for 7 days. ISO (100 mg/kg body weight) was subcutaneously injected into rats on 6th and 7th day to induce myocardial infarction (MI). Increased activity/levels of serum creatine kinase-MB (CK-MB), plasma thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes with decreased levels of plasma reduced glutathione (GSH), vitamin C, and vitamin E were observed in ISO-induced myocardial infarcted rats. Pre and cotreatment with thymol (7.5 mg/kg body weight) showed normalized activity of serum CK-MB and near normalized levels of plasma lipid peroxidation products, reduced GSH, vitamin C, and vitamin E in myocardial infarcted rats. Furthermore, the in vitro study on reducing power of thymol confirmed its potent antioxidant action. Thus, thymol protects ISO-induced MI in rats by its antilipid peroxidation and antioxidant properties.

A biochemical, electrocardiographic, electrophoretic, histopathological and in vitro study on the protective effects of (-)epicatechin in isoproterenol-induced myocardial infarcted rats.

(-) Epicatechin rich foods and (-) epicatechin improve cardiovascular function. Consumption of diets rich in flavonoids is associated with reduced risk of cardiovascular diseases. Oxidative stress resulting from increased production of free radicals associated with decreased levels of antioxidants in the myocardium plays a major role in the pathogenesis of myocardial infarction. This study aims to evaluate the preventive effects of (-) epicatechin on oxidative stress in isoproterenol-induced myocardial infarcted rats. Male Wistar rats were pretreated with (-) epicatechin (20mg/kg body weight) daily for 21 days. After pretreatment, isoproterenol (100mg/kg body weight) was injected into the rats at an interval of 24h for two days to induce myocardial infarction. Isoproterenol induced rat's electrocardiogram showed elevated ST segments and significant increase in the activity of serum creatine kinase-MB, level of serum troponin-T and increased intensities of serum lactate dehydrogenase 1 and 2-isoenzymes. The rats also showed significant increased levels of heart lipid peroxidation products and significant decreased activities of heart superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and levels of reduced glutathione. Pretreatment with (-) epicatechin revealed significant protective effects on all the biochemical parameters and electrocardiogram investigated. Histopathology of myocardium confirmed the present findings. The in vitro study on the effects of (-) epicatechin on scavenging free radical 1,1-diphenyl-2-picrylhydrazyl revealed the free radical scavenging potential of (-) epicatechin. Thus, (-) epicatechin exerts protective effects against isoproterenol-induced oxidative stress thereby reducing cardiac tissue damage by its free radical scavenging and antioxidant effects.

Antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic Wistar rats.

The present study aims to evaluate the antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic male Wistar rats. To induce diabetes mellitus, rats were injected with streptozotocin intraperitoneally at a single dose of 40mg/kg. Streptozotocin induced diabetic rats showed significant (P<0.05) increase in the levels of blood glucose, glycosylated haemoglobin and significant (P<0.05) decrease in the levels of plasma insulin, body weight and total haemoglobin. Diabetic rats also showed significant (P<0.05) decrease in the activity of hepatic hexokinase and significant (P<0.05) increase in the activities of glucose-6-phosphatase and fructose-1, 6-bisphosphatase. The pancreatic thiobarbituric acid reactive substances and lipid hydroperoxides were significantly (P<0.05) increased and the activities of pancreatic superoxide dismutase, catalase and glutathione peroxidase were significantly (P<0.05) decreased in diabetic rats. Oral treatment with gallic acid (10 and 20mg/kg) daily for a period of 21days showed significant (P<0.05) protective effects on all the biochemical parameters studied. Histopathology of pancreas confirmed the protective effects of gallic acid in diabetic rats. In vitro study also revealed the potent antioxidant effect of gallic acid. Thus, the study shows the antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic rats. The effect exerted by 20mg/kg body weight of gallic acid was more effective than 10mg/kg body weight of gallic acid.

Caffeic acid protects rat heart mitochondria against isoproterenol-induced oxidative damage.

Cardiac mitochondrial dysfunction plays an important role in the pathology of myocardial infarction. The protective effects of caffeic acid on mitochondrial dysfunction in isoproterenol-induced myocardial infarction were studied in Wistar rats. Rats were pretreated with caffeic acid (15 mg/kg) for 10 days. After the pretreatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-induced rats showed considerable increased levels of serum troponins and heart mitochondrial lipid peroxidation products and considerable decreased glutathione peroxidase and reduced glutathione. Also, considerably decreased activities of isocitrate, succinate, malate, α-ketoglutarate, and NADH dehydrogenases and cytochrome-C-oxidase were observed in the mitochondria of myocardial-infarcted rats. The mitochondrial calcium, cholesterol, free fatty acids, and triglycerides were considerably increased and adenosine triphosphate and phospholipids were considerably decreased in isoproterenol-induced rats. Caffeic acid pretreatment showed considerable protective effects on all the biochemical parameters studied. Myocardial infarct size was much reduced in caffeic acid pretreated isoproterenol-induced rats. Transmission electron microscopic findings also confirmed the protective effects of caffeic acid. The possible mechanisms of caffeic acid on cardiac mitochondria protection might be due to decreasing free radicals, increasing multienzyme activities, reduced glutathione, and adenosine triphosphate levels and maintaining lipids and calcium. In vitro studies also confirmed the free-radical-scavenging activity of caffeic acid. Thus, caffeic acid protected rat's heart mitochondria against isoproterenol-induced damage. This study may have a significant impact on myocardial-infarcted patients.

Pretreatment with quercetin ameliorates lipids, lipoproteins and marker enzymes of lipid metabolism in isoproterenol treated cardiotoxic male Wistar rats.

Lipids and lipoproteins play an important role in the pathology of myocardial infarction. This manuscript reports the preventive effect of quercetin on lipids, lipoproteins and electrocardiogram in isoproterenol treated cardiotoxic male Wistar rats. Quercetin (10mg/kg) was administered orally as pretreatment to Wistar rats daily for seven days. After pretreatment, rats were induced with myocardial infarction by subcutaneous injection of isoproterenol (100mg/kg) at an interval of 24h for two days. Quercetin pretreatment significantly (P<0.05) lowered ST-segment elevation and decreased the levels of lipid peroxidation products in plasma and heart in isoproterenol treated cardiotoxic rats. Quercetin pretreatment also significantly (P<0.05) reduced the levels of total cholesterol, triglycerides and free fatty acids in serum, heart and heart mitochondria and serum phospholipids in isoproterenol treated cardiotoxic rats. Significantly (P<0.05) increased levels of heart and heart mitochondria phospholipids were observed in quercetin pretreated isoproterenol treated cardiotoxic rats. It's pretreatment also significantly (P<0.05) reduced the levels of serum low-density lipoprotein and very low-density lipoprotein-cholesterol and significantly (P<0.05) increased serum high density lipoprotein-cholesterol in isoproterenol treated cardiotoxic rats. In addition, quercetin significantly (P<0.05) decreased the activity of 3-hydroxy-3-methyl glutaryl-Coenzyme A reductase in plasma and liver and significantly (P<0.05) increased the activity of liver lecithin cholesterol acyl transferase in isoproterenol treated cardiotoxic rats. In vitro study on total antioxidant activity clearly revealed the antioxidant property of quercetin. Thus, the antioxidant activity of quercetin inhibits lipid peroxidation and prevents accumulation of lipids, alterations in lipoproteins and electrocardiogram in isoproterenol treated cardiotoxic rats.

Preventive effect of S-allylcysteine on membrane-bound enzymes and glycoproteins in normal and isoproterenol-induced cardiac toxicity in male Wistar rats.

This study was aimed to evaluate the preventive role of S-allylcysteine (SAC) on creatine kinase-MB, iron, iron binding capacity, uric acid, total protein, membrane-bound enzymes such as sodium potassium-dependent adenosine triphosphatase, calcium-dependent adenosine triphosphatase and magnesium-dependent adenosine triphosphatase, and glycoproteins such as hexose, hexosamine, fucose and sialic acid in isoproterenol-induced myocardial infarction in rats. Male albino Wistar rats were pre-treated with SAC (50, 100 and 150 mg/kg) daily for a period of 45 days. After the treatment period, isoproterenol (150 mg/kg) was subcutaneously injected in rats at an interval of 24 hr for 2 days. Isoproterenol-induced rats showed significantly (P < 0.05) increased activities of serum creatine kinase-MB and calcium-dependent adenosine triphosphatase and magnesium-dependent adenosine triphosphatase in the heart, and the levels of iron and uric acid in serum and significantly (P < 0.05) decreased the levels of plasma iron binding capacity, plasma total protein, plasma albumin/globulin ratio and activity of sodium potassium-dependent adenosine triphosphatase in the heart. Isoproterenol induction also showed a significant increase in the levels of glycoproteins in serum and the heart. Pre-treatment with SAC (100 and 150 mg/kg) daily for a period of 45 days exhibited significant (P < 0.05) effect and altered these biochemical parameters positively. SAC (50, 100 and 150 mg/kg) treatment to normal rats did not exhibit any significant effect in any of the parameters studied. Thus, our study shows that SAC has a protective role in isoproterenol-induced myocardial infarction in rats. The observed effects might be due to the free radical scavenging, antioxidant and membrane stabilizing properties of SAC.

Cardioprotective effect of 'Marutham' a polyherbal formulation on isoproterenol induced myocardial infarction in Wistar rats.

Myocardial infarction is the number one killer disease in many parts of the world. The cardioprotective effect of Marutham, a polyherbal formulation on serum and heart tissue lipids, serum lipoproteins and heart membrane bound enzymes in isoproterenol induced myocardial infarction was studied in Wistar rats. Pretreatment with Marutham at different doses of 30, 60 and 90 mg kg(-1) to isoproterenol treated rats significantly prevented the altered lipid profile and membrane bound enzymes to near normal status. The results of our study showed the cardioprotective potential of Marutham on isoproterenol induced myocardial infarction in rats.