[Hepatoprotective effect of sodium molybdate on carbon tetrachloride-induced liver damage in rats]

The liver as a key organ of metabolism and excretion is constantly endowed with the task of detoxification. Hepatotoxicants can induce various disorders of the organ. Carbon tetrachloride [CCl4] is a potent hepatotoxin producing centrilobular hepatic necrosis and is widely used for animal models of hepatotoxicity. Molybdenum functions as a co-factor for a limited number of enzymes including xanthine oxidase, aldehyde oxidase and sulfite oxidase in mammals, and is believed to be an essential trace element in human and nutrition. The aim of the present study was to evaluate the protective effect of sodium molybdate against experimentally induced-CCl4 liver injury. Adult male rats were orally administered with different doses of sodium molybdate [0.05, 0.1 and 0.2g/kg bw/daily] along with CCl4 [50% CCl4, in olive oil, 1ml/kg bw, intrapertioneally] twice a week for 28 consecutive days. Biochemical parameters like alanine amino transferase, aspartate amino transferase, alkaline phosphatase and total protein levels in the serum were determined. In present study, the level of serum markers such as alanine amino transferase, aspartate amino transferase, and alkaline phosphatase were significantly increased in CCl4 treated rats. While Simultaneous treatment of sodium molybdate at doses 0.05, 0.1 and 0.2g/kg bw significantly decreased alanine amino transferase, aspartate amino transferase and alkaline phosphatase at the dependent dosage manner. Moreover, it had no effect on serum total protein levels. The results of this study demonstrate the hepatoprotective effect of molybdenum and thus scientifically supports the use of this trace element for treatment of liver disorders

Hypoglycemic effect of ethanolic extract of Carum carvi L. seeds in normal and streptozotocin-induced diabetic rats

Herbal medicine has been used for many years by different cultures around the world for the treatment of diabetes. The hypoglycemic effect of caraway ethanolic extract [Carum carvi L.] was investigated in normal and streptozotocin-induced diabetic rats. Intraperitoneal administration of caraway ethanolic extract seeds [0.1, 0.2, 0.4 and 0.6 g/kg body wt.] on the level of serum glucose and insulin in normal and streptozotocin-induced diabetic rats were evaluated. Before administration and 1, 3 and 5 h after administrations of the ethanolic extract, blood samples were drawn from the retro-orbital sinus. Serum glucose and insulin levels were determined. The results showed that the caraway ethanolic extract seeds at doses 0.2, 0.4 and 0.6 g/kg body wt. significantly decreased serum glucose and insulin in diabetic rats in 3 and 5 h but not in healthy rats. It could be proofed that the traditional use of caraway as a hypoglycemic agent is justified and that extract from this plant show a dose-dependent hypoglycemic activity

Control of environmental health and removal of rats by alpha[2]-adrenergic antagonist and potassium channel blocker

In the present study, it is shown that in vivo oral administration of glibenclamide [1-10 mg/kg/day], an adenosine triphosphate -sensitive potassium channel blocker, and yohimbine [1-5 mg/kg/day], an alpha 2-adrenoceptor antagonist, potently reduced glycemia in male rats. Diazoxide [1-45 mg/kg/day], a potassium channel opener, and clonidine [0.05-0.5 mg/kg/day], an alpha 2- adrenoceptor agonist, antagonized the effects of glibenclamide and yohimbine respectively. Administration of glibenclamide and yohimbine separately decreased the serum glucose levels, so it was expected that coadministration of these two drugs significantly decreased this parameter in fasted animals. It is well known that glibenclamide blocks the potassium channels and it is likely that, yohimbine also blocks these channels, but according to our data, it seems that yohimbine acts via a different binding site to that of glibenclamide. In this research it is also observed that administration of yohimbine and glibenclamide causes death in rats, it seems that these drugs causes death in the experimental animals by lowering blood glucose level, which were the aim of this study and could be applied as a way to control the environmental health by abolishing rats