Kodukkur Viswanathan Pugalendi

Effect of chrysin on hepatoprotective and antioxidant status in D-galactosamine-induced hepatitis in rats.

Chrysin is a natural, biologically active compound present in many plants and possesses potent anti-inflammatory, anticancer and antioxidation properties. This work was designed to investigate the effect of chrysin, on the hepatoprotective efficacy in d-galactosamine-intoxication rats. d-galactosamine-induced toxicity was manifested by the elevation of serum hepatic marker enzyme activities (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase) and the lipid peroxidation process and by decreasing the antioxidant capacity of the plasma, erythrocyte and tissues. Treatment with chrysin (25, 50 and 100mg/kg body weight) decreased hepatic marker enzyme activities and lipid peroxidation products such as thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes, increased the activities of free-radical scavenging enzymes superoxide dismutase, catalase and glutathione peroxidase and the levels of non-enzymatic antioxidants reduced glutathione, vitamin C and vitamin E. These findings demonstrate that chrysin acts as a hepatoprotective and antioxidant agent against d-galactosamine-induced hepatotoxicity.

A novel compound from Casearia esculenta (Roxb.) root and its effect on carbohydrate metabolism in streptozotocin-diabetic rats.

Casearia esculenta root (Roxb.) is widely used in traditional system of medicine to treat diabetes in India. An active compound 3-hydroxymethyl xylitol (3-HMX) has been isolated and its optimum dose has been determined in a short duration study and patented. In the present study, the long-term effect of 3-HMX in type 2 diabetic rats has been investigated. An optimum dose of 3-HMX (40 mg/kg body weight) was orally administered for 45 days to streptozotocin-diabetic rats for the assessment of glucose, insulin, hemoglobin (Hb), glycated hemoglobin (HbA(1c)), hepatic glycogen, and activities of carbohydrate metabolizing enzymes, such as glucokinase, glucose 6-phosphatase, fructose 1,6-bisphosphatase and glucose-6-phosphate dehydrogenase and hepatic marker enzymes, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gammaglutamyl transferase (GGT) in normal and streptozotocin-diabetic rats. 3-HMX at 40 mg dose produced similar effects on all biochemical parameters studied as that of glibenclamide, a standard drug. Histological study of pancreas also confirmed the biochemical findings. These results indicate that 3-hydroxymethyl xylitol, the compound from C. esculenta, possesses antihyperglycemic effect on long-term treatment also.

Cardioprotective effect of oleanolic acid on isoproterenol-induced myocardial ischemia in rats

This study was designed to investigate the protective effect of oleanolic acid (OA) against isoproterenol-induced myocardial ischemia in rat myocardium. Wistar strain rats were pretreated with OA (20, 40, and 60 mg/kg, s.c) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, sc for 2 consecutive days). Heart were excised from the experimental animals and assessed for the activities of marker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HP) and conjugated dienes (CD)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFA) and phospholipids (PL)], and membrane-bound ATPase enzymes (total ATPase, Na+K+ATPase, Ca2+ATPase, and Mg2+ATPase). Troponin T and I were estimated in plasma. Leakage of cardiac markers, elevated lipid peroxidation with increased lipid profiles and decreased activities of membrane-bound ATPase enzymes were confirmed the severe myocardial damage occurring as a consequence of isoproterenol-induced ischemia, and they also showed the significant improvement effected by oleanolic acid pretreatment. These findings provided evidence that oleanolic acid was found to be protecting rat myocardium against ischemic insult and the protective effect could attribute to its anti-oxidative, anti-hyperlipedemic, and anti-arrhythmic properties as well as its membrane-stabilizing action.

Effect of Piper betle Leaf Extract on Alcoholic Toxicity in the Rat Brain

The protective effect of Piper betle, a commonly used masticatory, has been examined in the brain of ethanol-administered Wistar rats. Brain of ethanol-treated rats exhibited increased levels of lipids, lipid peroxidation, and disturbances in antioxidant defense. Subsequent to the experimental induction of toxicity (i.e., the initial period of 30 days), aqueous P. betle extract was simultaneously administered in three different doses (100, 200, and 300 mg kg(-1)) for 30 days along with the daily dose of alcohol. P. betle coadministration resulted in significant reduction of lipid levels (free fatty acids, cholesterol, and phospholipids) and lipid peroxidation markers such as thiobarbituric acid reactive substances and hydroperoxides. Further, antioxidants, like reduced glutathione, vitamin C, vitamin E, superoxide dismutase, catalase, and glutathione peroxidase, were increased in P. betle-coadministered rats. The higher dose of extract (300 mg kg(-1)) was more effective, and these results indicate the neuroprotective effect of P. betle in ethanol-treated rats.

Effect of carvacrol on hepatic marker enzymes and antioxidant status in d-galactosamine-induced hepatotoxicity in rats

Carvacrol (2‐methyl‐5‐(1‐methylethyl)‐phenol) is a predominant monoterpenic phenol which occurs in many essential oils of the family Labiatae including Origanum, Satureja, Thymbra, Thymus, and Corydothymus species. This study was designed to investigate the hepatoprotective and antioxidant properties of carvacrol on d‐galactosamine (D‐GalN)‐induced hepatotoxicity and oxidative damage in male albino Wistar rats. D‐GalN hepatotoxic rats exhibited elevation in the activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma‐glutamyl transpeptidase, and lipidperoxidative markers such as thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides. Activities of enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and the levels of non‐enzymatic antioxidants (vitamin C, vitamin E, and reduced glutathione) in the plasma, erythrocytes, liver, and kidney decreased in the hepatotoxic rats. Oral administration of carvacrol for 21 days brought these parameters towards normal. The biochemical observations were supported by histological studies of rat liver and kidney tissues. These results suggest that carvacrol could afford a significant hepatoprotective and antioxidant effect against D‐GalN‐induced rats.

Influence of Piper betle on hepatic marker enzymes and tissue antioxidant status in ethanol-treated Wistar rats.

Piper betle L. is a commonly used masticatory in Asia. This study was carried out to investigate the hepatoprotective and antioxidant properties of P. betle, using ethanol intoxication as a model of hepatotoxic and oxidative damage. Ethanol-treated rats exhibited elevation of hepatic marker enzymes and disturbances in antioxidant defense when compared with normal rats. Oral administration of P. betle extract (100, 200, or 300 mg/kg body weight) for 30 days significantly (P <.05) decreased aspartate aminotransferase (AST), alanine aminotransferase (ALT), thiobarbituric acid reactive substances (TBARS), and lipid hydroperoxides in ethanol treated rats. The extract also improved the tissue antioxidant status by increasing the levels of nonenzymatic antioxidants (reduced glutathione, vitamin C, and vitamin E) and the activities of free radical-detoxifying enzymes such as superoxide dismutase, catalase, and glutathione peroxidase in liver and kidney of ethanol-treated rats. The highest dose of P. betle extract (300 mg/kg body weight) was most effective. The results were comparable with the known hepatoprotective drug, silymarin. These results indicate that P. betle could afford a significant hepatoprotective and antioxidant effect.

Antihyperglycemic effect of 18β-glycyrrhetinic acid, aglycone of glycyrrhizin, on streptozotocin-diabetic rats

The study was designed to investigate the antihyperglycemic effect of 18 beta-glycyrrhetinic acid, aglycone of glycyrrhizin, on streptozotocin-diabetic rats. Diabetes was induced in adult male albino rats of the Wistar strain, weighing 180-200 g, by administration of streptozotocin (40 mg/kg of body weight) intraperitoneally. Diabetic rats showed increase of plasma glucose and glycosylated haemoglobin (HbA(1c)) and a decrease of plasma insulin and haemoglobin (Hb). Activities of gluconeogenic enzymes such as glucose 6-phosphatase, fructose 1, 6-bisphosphatase increased and glucokinase, glucose 6-phosphate dehydrogenase decreased in the liver along with glycogen. Oral administration of 18 beta-glycyrrhetinic acid (50, 100, or 200 mg/kg/body weight) or glibenclamide (600 microg/kg/body weight) in 5% dimethyl sulfoxide, for 45 days, prevented the above changes and improved towards normalcy. No significant effect was observed in normal rats treated with 18 beta-glycyrrhetinic acid (200 mg/kg/body weight). Thus, our results show that 18 beta-glycyrrhetinic acid at 100 mg/kg of body weight possesses a potential antihyperglycemic effect that is comparable with glibenclamide.

Influence of chrysin on hepatic marker enzymes and lipid profile against D-galactosamine-induced hepatotoxicity rats.

Chrysin is a flavonoid that exists in nature and is the major component of some traditional medicinal herbs. We investigated the hepatoprotective and antihyperlipidaemic potential of chrysin against D-galactosamine (a single intraperitoneal injection 400 mg/kg BW) induced hepatotoxicity in male albino Wistar rats. D-GalN rats exhibited an increased hepato and nephro toxicity marker activities aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma glutamyl transpeptidase and total bilirubin level while urea, uric acid and creatinine and lipid profile. It also negatively affected the serum total protein, albumin and A/G ratio. Rats treated with chrysin at different concentrations (25, 50 and 100 mg/kg BW) caused a significant improvement in serum protein level, decreased hepato and nephro toxicity markers. It also decreased the levels of very low density lipoprotein cholesterol and low density lipoprotein cholesterol while high density lipoprotein cholesterol significantly increased. It also decreased the levels of total cholesterol, phospholipids, triglycerides, free fatty acids in the plasma and tissues of liver and kidney. The effect of chrysin (25 mg/kg) is comparable with silymarin, a known hepatoprotective drug. Chrysin thus exhibits hepatoprotective and antihyperlipidaemic activity.

Hypolipidemic activity of 18β-glycyrrhetinic acid on streptozotocin-induced diabetic rats

Diabetes mellitus is a significant risk factor for cardiovascular complications. This study was undertaken to investigate the effect of 18beta-glycyrrhetinic acid on plasma glucose and plasma and tissue lipid profiles in streptozotocin-induced diabetic rats. Diabetes was induced in adult male albino rats of the Wistar strain, weighing 180-200 g, by administration of streptozotocin (40 mg/kg of body weight) intraperitoneally. Rats were randomly divided into seven groups. Group I: control animals (normal, nondiabetic animals), Group II: 18beta-glycyrrhetinic acid control, Group III: streptozotocin-diabetic, untreated animals; Groups IV, V and VI: streptozotocin-diabetic animals given 50, 100 and 200 mg 18beta-glycyrrhetinic acid, and Group VII: streptozotocin-diabetic animals given glibenclamide. The levels of total cholesterol, triglycerides, free fatty acids, and phospholipids, were assayed in the plasma besides lipoprotein-cholesterol (high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C) and very low density lipoprotein-cholesterol (VLDL-C)) and tissues (liver, kidney and heart). Total cholesterol, triglyceride, free fatty acid, and phospholipid (LDL-C and VLDL-C in plasma only) levels increased in plasma and tissues significantly, while plasma HDL-cholesterol significantly decreased in diabetic rats. Treatment with 18beta-glycyrrhetinic acid prevented the above changes and improved towards normalcy. Thus administration of 18beta-glycyrrhetinic acid is able to reduce hyperglycemia and hyperlipidemia related to the risk of diabetes mellitus.

Effect of ursolic acid on cardiac marker enzymes, lipid profile and macroscopic enzyme mapping assay in isoproterenol-induced myocardial ischemic rats

This study investigates the antihyperlipidemic effect of ursolic acid (UA) on isoproterenol (ISO) induced male albino Wistar rats. Myocardial ischemia was induced by subcutaneous injection of ISO (85 mg/kg BW) twice at an interval of 24 h, for two consecutive days. A significant increase in the activities of the serum marker enzymes [creatine kinase, creatine kinase-MB and lactate dehydrogenease (LDH)], a prominent expression of LDH 1 and LDH 2 isoenzymes, increased levels of plasma total cholesterol (TC), low density lipoprotein-cholesterol, very low density lipoprotein-cholesterol, triglycerides (TG), free fatty acids (FFA), phospholipids (PL) and atherogenic index and decreased level of high density lipoprotein-cholesterol were observed in ISO-induced rats. The levels of TC, TG and FFA increased and the level of PL decreased in the heart tissue of ISO-induced rats. Further, there was an increased DNA damage (Comet assay) and myocardium infarct size as observed by staining with triphenyltetrazolium chloride (TTC). UA was administered subcutaneously for 7 days at a dose of 40 mg/kg BW. UA administration to ischemic rats brought all these parameters to near normality showing the protective effect of UA on ISO-induced rats.