Preventive effects of zingerone on altered lipid peroxides and nonenzymatic antioxidants in the circulation of isoproterenol-induced myocardial infarcted rats.

The present study was designed to evaluate the preventive effects of zingerone on circulatory lipid peroxides and nonenzymatic antioxidants in isoproterenol-induced myocardial infarcted rats. Rats were pretreated with zingerone (6 mg/kg body weight) daily for a period of 14 days and were then induced myocardial infarction with isoproterenol (100 mg/kg body weight) on 15th and 16th day. Increased intensities of serum lactate dehydrogenase isoenzymes 1 and 2 bands enhanced plasma lipid peroxidation products and lowered nonenzymatic antioxidant system were noted in isoproterenol-induced rats. Pretreatment with zingerone daily for 14 days revealed significant preventive effects on the electrophoretic and biochemical parameters evaluated in isoproterenol-induced rats. Furthermore, the in vitro study confirmed the potent antioxidant activity of zingerone. The results of our study showed that zingerone protected the rat's heart against isoproterenol-induced myocardial infarction by its antioxidant effect.

Preventive effects of vanillic acid on lipids, bax, bcl-2 and myocardial infarct size on isoproterenol-induced myocardial infarcted rats: a biochemical and in vitro study.

We made an attempt to evaluate the preventive effects of vanillic acid on isoproterenol-induced myocardial infarcted rats. Rats were pretreated with vanillic acid (5 and 10 mg/kg) daily for 10 days. After pretreatment, rats were injected with isoproterenol (100 mg/kg) at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol induction increased the activity of serum creatine kinase-MB and increased the levels of serum and heart cholesterol, triglycerides, free fatty acids in rats. It increased the levels of serum low density and very low density lipoprotein cholesterol and decreased the levels of high-density lipoprotein cholesterol. Also, the activity of 3-hydroxy-3methyl glutaryl-coenzyme-A-reductase in the plasma and liver was increased, and lecithin cholesterol acyl transferase activity in the plasma and liver was decreased in isoproterenol-induced rats. Furthermore, isoproterenol-induced rats showed a decrease in myocardial expression of B-cell leukemia/lymphoma-2(bcl-2) gene and an increase in myocardial expression of bcl-2 associated-x (bax)-gene. Vanillic acid pretreated isoproterenol-induced rats positively altered all the above-mentioned biochemical parameters. Vanillic acid pretreatment also reduced myocardial infarct size in myocardial infarcted rats. In vitro study confirmed the potent free radical scavenging effect of vanillic acid. The observed effects are due to free radical scavenging effects of vanillic acid. This study may have a significant impact on myocardial infarcted patients.

Protective effects of rutin on mitochondrial damage in isoproterenol-induced cardiotoxic rats: an in vivo and in vitro study.

Consumption of diets rich in flavonoids is associated with reduced risk of cardiovascular diseases such as myocardial infarction. Cardiotoxicity was induced in rats by subcutaneous injection of isoproterenol at an interval of 24 h for 2 days. Isoproterenol-induced rats showed a significant increase in the levels of heart mitochondrial lipids, lipid peroxidation products, calcium and a significant decrease in the activities/levels of mitochondrial antioxidants, enzymes and adenosine triphosphate. Isoproterenol-induced rats also showed an increase in the intensities of serum lactate dehydrogenase-1 and 2 isoenzyme bands. Pretreatment with rutin at the dose of 80 mg/kg daily for 42 days to isoproterenol-induced rats prevented all the biochemical alterations. Transmission electron microscopic study also confirmed the protective effects of rutin on the structure of heart mitochondria. Thus, rutin reduced the extent of mitochondrial damage induced by isoproterenol and prevented cardiac mitochondrial dysfunction. The possible mechanisms for the observed effects of rutin could be due to scavenging free radicals, lowering lipid peroxides, lipids and calcium, improving multienzyme activities, glutathione levels, adenosine triphosphate levels, thereby improving cardiac mitochondrial structure and function. This study may have a significant impact on myocardial infarcted patients.

Preventive effect of caffeic acid on lysosomal dysfunction in isoproterenol-induced myocardial infarcted rats.

We evaluated the preventive effect of caffeic acid (CA) on lysosomal enzymes in isoproterenol (ISO)-treated myocardial infarcted rats. Male albino Wistar rats were pretreated with CA (15 mg/kg) daily for a period of 10 days. After the pretreatment period, ISO (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of serum creatine kinase-MB and lactate dehydrogenase was increased significantly (P < 0.05) in ISO-induced myocardial infarcted rats. The levels of plasma thiobarbituric acid reactive substances and lipid hydroperoxides were significantly (P < 0.05) increased, and the level of plasma-reduced glutathione was significantly (P < 0.05) decreased in ISO-induced myocardial infarcted rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly (P < 0.05) in the serum and heart of ISO-induced myocardial infarcted rats. ISO induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in different fractions except cytosol. Pretreatment with CA (15 mg/kg) to ISO-treated rats significantly (P < 0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes in the serum, heart, and subcellular fractions. Oral treatment with CA (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study showed that CA prevented the lysosomal membrane damage against ISO-induced myocardial infarction. The observed effects of CA are due to membrane-stabilizing, antilipo peroxidative, and antioxidant effects.

Protective effect of caffeic acid on cardiac markers and lipid peroxide metabolism in cardiotoxic rats: an in vivo and in vitro study.

Myocardial infarction affects a large population in the world. Lipid peroxide metabolism plays an important role in the pathology of myocardial infarction. This study aims to evaluate the preventive effect of caffeic acid on lipid peroxides, antioxidants, cardiac marker enzymes, and histopathological findings in isoproterenol (ISO)-induced myocardial-infarcted male Wistar rats. Myocardial infarction was induced in rats by subcutaneous injection of ISO (100 mg/kg) at an interval of 24 hours for 2 days. The ISO-induced rats showed significant increase in the levels of thiobarbituric acid reactive substances, lipid hydroperoxides in the heart, plasma uric acid, and serum cardiac marker enzymes, and significant decrease in the activities of heart superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and the levels of reduced glutathione, vitamin E, and vitamin C in the plasma and heart. Oral pretreatment with caffeic acid (15 mg/kg) daily for 10 days showed significant decrease in the levels of serum cardiac marker enzymes, heart lipid peroxidation products and plasma uric acid and significant increase in the levels of antioxidant system. Histopathology of myocardium also confirmed the protective effect of caffeic acid in myocardial-infarcted rats. In vitro study on total antioxidant activity (2,2'-azinobis-[3-ethylbenzothiazoline-6-sulfonic acid](+) assay) confirmed the strong antioxidant action of caffeic acid. Thus, the present study revealed that caffeic acid ameliorates cardiac damage in ISO-induced myocardial infarction by maintaining lipid peroxide metabolism due to its free radical scavenging and antioxidant effects. A diet containing caffeic acid may be beneficial to myocardial infarction.

Pretreatment with a combination of quercetin and alpha-tocopherol ameliorates adenosine triphosphatases and lysosomal enzymes in myocardial infarcted rats.

AIMS: Membrane bound adenosine triphosphatases (ATPases) and lysosomal enzymes play an important role in the pathology of myocardial infarction. This study was aimed to evaluate the combined preventive effects of quercetin and alpha-tocopherol on membrane bound ATPases and lysosomal enzymes in isoproterenol induced myocardial infarcted rats. MAIN METHODS: Male Wistar rats were pretreated with a combination of quercetin (10mg/kg) and alpha-tocopherol (10mg/kg) daily for 14 days. After the pretreatment period, isoproterenol (100mg/kg) was injected to rats at an interval of 24h for two days to induce myocardial infarction. The activities of ATPases and lysosomal enzymes were assayed. KEY FINDINGS: Isoproterenol treated rats showed decreased levels of heart creatine kinase and lactate dehydrogenase. The activity of sodium potassium adenosine triphosphatase was decreased and the activities of magnesium adenosine triphosphatase and calcium adenosine triphosphatase were increased in isoproterenol treated rats. Also, the activities of beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and D were increased (serum and heart), but the activities of beta-glucuronidase and cathepsin-D were decreased in lysosomal fraction and increased in cytosolic fraction of the heart in isoproterenol treated rats. Furthermore, the heart lipid peroxidation products were increased in isoproterenol treated rats. Combined pretreatment with quercetin and alpha-tocopherol to isoproterenol treated rats normalized all the biochemical parameters studied. The observed effects are due to their membrane stabilizing property and this property might be due to decreased lipid peroxidation. SIGNIFICANCE: Our study demonstrated that combined pretreatment was better than single pretreatment. This study may have significant impact on myocardial infarcted patients.

Combined effects of quercetin and alpha-tocopherol on lipids and glycoprotein components in isoproterenol induced myocardial infarcted Wistar rats.

This study was aimed to evaluate the combined effects of quercetin and alpha-tocopherol on lipid metabolism and glycoprotein components in isoproterenol induced myocardial infarction in Wistar rats. Myocardial infarction in rats was induced by isoproterenol (100mg/kg) at an interval of 24h for 2 days. Quercetin (10 mg/kg) and alpha-tocopherol (10 mg/kg) were given to rats as pretreatment for 14 days orally using an intragastric tube. Quercetin and alpha-tocopherol significantly reduced the levels of cholesterol, triglycerides and free fatty acids in the serum and heart and serum phospholipids and significantly increased the levels of heart phospholipids in isoproterenol induced rats. They also significantly decreased the activity of plasma and liver 3-hydroxy-3-methylglutaryl-coenzyme-A reductase and increased the activity of plasma and liver lecithin cholesterol acyl transferase in isoproterenol treated rats. In addition to this, they also significantly reduced the levels of hexose, hexosamine, fucose and sialic acid in the serum and heart of isoproterenol treated rats. Quercetin and alpha-tocopherol also showed significant decrease in plasma lipid peroxidation products (thiobarbituric acid reactive substances and lipid hydroperoxides). Pretreatment with quercetin alone and alpha-tocopherol alone showed significant effect in all the biochemical parameters in myocardial infarcted rats. But, combined pretreatment with quercetin and alpha-tocopherol normalized all the above mentioned biochemical parameters in isoproterenol treated myocardial infarction in rats. Thus, the experiment clearly showed that quercetin and alpha-tocopherol prevented the accumulation of lipids and glycoprotein components in myocardial infarcted rats by their anti-lipid peroxidative effect. This study also showed that combined pretreatment was better than single pretreatment.

Cardioprotective effect of gallic acid on cardiac troponin-T, cardiac marker enzymes, lipid peroxidation products and antioxidants in experimentally induced myocardial infarction in Wistar rats.

Currently there has been an increased interest globally to identify antioxidant compounds that are pharmacologically potent and have low or no side effects for use in preventive medicine. This study was designed to evaluate the protective effect of gallic acid on cardiac marker enzymes, troponin-T, LDH-isoenzyme pattern, lipid peroxidation products and antioxidant status in isoproterenol (ISO)-induced myocardial infarction in male Wistar rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, ISO (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days. ISO-induced myocardial damage was indicated by increased activities of marker enzymes such as creatine kinase, creatine kinase-MB, aspartate transaminase, alanine transaminase and lactate dehydrogenase in serum and the levels of troponin-T in the serum. Increased LDH-isoenzyme bands (LDH-1 and LDH-2) were also observed in serum of ISO-induced rats. In addition to these diagnostic markers, the levels of lipid peroxidation products in plasma and the heart were significantly (P<0.05) increased and the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase in the heart and non-enzymic antioxidants such as glutathione, vitamin C and E in plasma and the heart were significantly (P<0.05) decreased in ISO-induced rats. The level of uric acid in plasma was significantly (P<0.05) increased in ISO-treated rats. Gallic acid pretreatment showed significant protective effect on all the biochemical parameters studied. Histopathological findings of gallic acid pretreated myocardial infarcted heart confirmed the biochemical findings of this study. Thus, gallic acid protects the myocardium against isoproterenol-induced oxidative stress.

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.

Antihyperlipidemic effect of D-pinitol on streptozotocin-induced diabetic Wistar rats.

D-pinitol (3-O-methyl-chiroinositol), an active principle of the traditional antidiabetic plant, Bougainvillea spectabilis, is claimed to exert insulin-like effects. This study was undertaken to evaluate the effect of D-pinitol on lipids and lipoproteins in streptozotocin (STZ)-induced diabetic Wistar rats. Rats were made type II diabetic by single intraperitoneal injection of STZ at a dose of 40 mg/kg body weight. STZ-induced diabetic rats showed significant (p < 0.05) increase in the levels of blood glucose and total cholesterol, triglycerides, free fatty acids, and phospholipids in serum, liver, kidney, heart, and brain. The levels of low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol were significantly increased, and the level of high-density lipoprotein (HDL) cholesterol was significantly decreased in diabetic rats Oral administration of D-pinitol to STZ-induced diabetic rats showed significant (p < 0.05) decrease in the levels of blood glucose and total cholesterol, triglycerides, free fatty acids, and phospholipids in serum, liver, kidney, heart, and brain. The D-pinitol also lowered significantly (p < 0.05) LDL and VLDL cholesterol levels and increased significantly (p < 0.05) HDL cholesterol levels in the serum of diabetic rats. Thus, the present study clearly showed the antihyperlipidemic effect of D-pinitol in STZ-induced type II diabetic rats.

Combined treatment with naringin and vitamin C ameliorates streptozotocin-induced diabetes in male Wistar rats.

Diet and nutrition have substantial impact on reducing the incidence of diabetes mellitus, where oxidative stress is an important etiopathological factor. The combined protective role of low dose of naringin (15 mg kg(-1)) and vitamin C (25 mg kg(-1)) and high dose of naringin (30 mg kg(-1)) and vitamin C (50 mg kg(-1)) on streptozotocin (STZ)-induced toxicity was studied in male Wistar rats. To induce type II diabetes mellitus, rats were injected with STZ intraperitoneally at a dose of 45 mg kg(-1) body weight. STZ-induced diabetic rats showed significant increase in blood glucose, water intake, food intake and glycated hemoglobin and significant decrease in plasma insulin, total hemoglobin, body weight and liver glycogen. Diabetic rats also showed significant decrease in the activity of hexokinase and significant increase in the activities of glucose-6-phosphatase and fructose-1,6-bisphosphatase in liver and kidney. The levels of plasma thiobarbituric acid reactive substances, lipid hydroperoxides and vitamin E were elevated while the level of reduced glutathione was decreased in diabetic rats. Glycoprotein components such as hexose, hexosamine, fucose and sialic acid were increased in plasma, liver and kidney of diabetic rats. Oral administration of high doses of naringin (30 mg kg(-1)) and vitamin C (50 mg kg(-1)) to diabetic rats for a period of 21 days normalized all the above-mentioned biochemical parameters. The effect exerted by naringin (30 mg kg(-1)) and vitamin C (50 mg kg(-1)) was similar to the effect exerted by insulin (6 units kg(-1)). Thus, our study shows the antihyperglycemic and antioxidant effects of naringin and vitamin C in STZ-induced type II diabetes mellitus in rats.

Preventive effect of (-)epigallocatechin-gallate (EGCG) on lysosomal enzymes in heart and subcellular fractions in isoproterenol-induced myocardial infarcted Wistar rats.

This study was aimed to evaluate the preventive role of (-)epigallocatechin-gallate (EGCG) on lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarcted rats. Male albino Wistar rats were pretreated with EGCG (30 mg/kg) daily for a period of 21 days. After the treatment period, ISO (100 mg/kg) was subcutaneously injected to rats at intervals of 24h for 2 days. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly (P<0.05) in serum and the heart of ISO-induced rats. ISO-induction also resulted in decreased stability of membranes, which was reflected by decreased activities of beta-glucuronidase and cathepsin-D in mitochondrial, nuclear, lysosomal and microsomal fractions. Pretreatment with EGCG daily for a period of 21 days to ISO-induced rats prevented the changes in the activities of these enzymes. Oral treatment with EGCG (30 mg/kg) to normal control rats did not show any significant effect in all the biochemical parameters studied. Thus, the results of our study shows that EGCG protects the lysosomal membrane against ISO-induced cardiac damage. The observed effects might be due to the free radical scavenging and membrane stabilizing properties of EGCG.

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 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 S-allylcysteine on lipid peroxides and antioxidants in normal and isoproterenol-induced cardiotoxicity in rats: a histopathological study.

The consumption of diets rich in plant foods are associated with a reduced risk of cardiovascular diseases. This study was aimed to evaluate the role of S-allylcysteine (SAC) in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (150 mg/kg) to Wistar rats showed a significant decrease in the activities of marker enzymes such as creatine kinase, lactate dehydrogenase, aspartate and alanine transaminases in heart and a significant increase in the levels of thiobarbituric acid reactive substances and lipid hydroperoxides in plasma and heart. ISO-induced rats also showed a significant decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione S-transferase in heart and the levels of glutathione and ascorbic acid in plasma and heart. Oral administration of SAC (100 and 150 mg/kg) to ISO-treated rats daily for a period of 45 days caused a significant increase in the activities of marker enzymes and improved the antioxidant status by decreasing lipid peroxidative products and increasing the activities of antioxidant enzymes and the levels of nonenzyomic antioxidants. Administration of SAC to normal rats did not show any significant effect. Histopathological findings of the myocardial tissue showed a protective role of SAC in ISO-treated rats. The effect at a dose of 150 mg/kg of SAC was more pronounced than that of the dose 100mg/kg and brought back all the parameters to near normal. The effect exerted by 100 mg/kg of SAC was similar to that of alpha-tocopherol (60 mg/kg). The results of our study show that SAC possesses antioxidant activity in ISO-induced experimental MI.

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.

Effect of aqueous Enicostemma littorale Blume extract on key carbohydrate metabolic enzymes, lipid peroxides and antioxidants in alloxan-induced diabetic rats.

The present study investigates the effect of oral administration of an aqueous Enicostemma littorale whole plant extract on some key carbohydrate metabolic enzymes and antioxidant defence in alloxan-induced diabetes in rats. Rats were rendered diabetic by alloxan (150 mgkg(-1) body weight) administration. Oral administration of E. littorale extract for 45 days increased the activity of hexokinase and decreased the activities of glucose 6-phosphatase and fructose 1,6-bisphosphatase significantly in the serum, liver and kidney of diabetic rats. The extract lowered the concentration of thiobarbituric acid reactive substances and lipid hydroperoxides significantly in brain and increased it significantly in heart in diabetic rats. E. littorale administration increased the concentration of reduced glutathione and the activity of glutathione peroxidase in diabetic rats. The activities of superoxide dismutase and catalase were increased significantly by E. littorale treatment in diabetic rats. The effect of a 2 g kg(-1) dose was greater than that of a 1 gkg(-1) dose. Insulin (6 units kg(-1)) normalized all the parameters in diabetic rats. Our study has provided evidence for the antidiabetic activity of E. littorale aqueous extract. This study can also be extrapolated to clinical studies in future.

The effect of Aegle marmelos fruit extract in streptozotocin diabetes: a histopathological study.

Aegle marmelos Correa. (Bael) fruit exhibit antidiabetic, antihyperlipidaemic and antioxidant properties. This study was designed to elucidate the protective effect of an aqueous extract of Aegle marmelos fruits on the histopathology of the pancreas in streptozotocin-induced diabetic rats. Oral administration of Aegle marmelos fruit extract at doses of 125 and 250 mg/kg twice daily to diabetic rats for a period of 30 days resulted in a significant increase in body weight, weight of the pancreas and insulin levels associated with a significant decrease in fasting blood glucose levels. The fruit extract treated groups showed improved functional state of the pancreatic ss-cells and partially reversed the damage caused by streptozotocin to the pancreatic islets. The findings of our study indicate that Aegle marmelos fruit extract exhibits protective effects on the pancreas. The effects observed in the fruit extract treated animals were better those in animals treated with glibenclamide (300 microg/kg).

Restoration of antioxidant defence by ethanolic Tinospora cordifolia root extract in alloxan-induced diabetic liver and kidney.

The present study investigates the effect of oral administration of an alcoholic extract of Tinospora cordifolia roots on antioxidant defence in alloxan-induced diabetes in rats. A significant increase in the concentration of thiobarbituric acid reactive substances (TBARS) in liver and kidney was observed in diabetic rats. Decreased concentration of glutathione (GSH) and decreased activities of superoxide dismutase (SOD), and catalase in liver and kidney of diabetic rats were also noted. Alcoholic Tinospora cordifolia root extract (TCREt) administered at a dose of 100 mg/kg body weight to diabetic rats orally for six weeks normalized the antioxidant status of liver and kidney. The effect of Tinospora cordifolia root extract was more potent than glibenclamide (600 microg/kg body weight). Insulin (6 units/kg) restored all the parameters to normal status.

Antidiabetic and antihyperlipidaemic effect of alcoholic Syzigium cumini seeds in alloxan induced diabetic albino rats.

Syzigium cumini, commonly known as 'jamun', is widely used in different parts of India for the treatment of diabetes mellitus. The present study was designed to evaluate the antidiabetic and antihyperlipidaemic effect of an alcoholic extract of Syzigium cumini seeds (JSEt) in alloxan diabetic rats. Diabetes was induced by single intraperitoneal injection of alloxan (150 mg kg(-1) body weight). Oral administration of alcoholic JSEt to diabetic rats at a dose of 100 mg kg(-1) body weight resulted in a significant reduction in blood glucose and urine sugar and lipids in serum and tissues in alloxan diabetic rats. The extract also increases total haemoglobin. The extract brought back all the parameters to normal levels. The effect of alcoholic JSEt was similar to that of insulin. Thus, our investigation clearly shows that alcoholic JSEt has both antidiabetic and antihyperlipidaemic effects.