Activity of Cassia auriculata leaf extract in rats with alcoholic liver injury

This study was undertaken to investigate the effect of Cassia auriculata leaf extract on tissue lipid peroxidation and antioxidant status in experimental hepatotoxicity. Administering ethanol to rats for 60 days resulted in significantly elevated levels of serum total bilirubin, aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) as compared with those of the experimental control rats. Significantly elevated levels of tissue thiobarbituric acid reactive substances (TBARS), hydroperoxides and lowered activities of superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) were also observed on alcohol treatment as compared with those of experimental control rats. Concentration of serum non-enzymic antioxidants such as vitamin E and vitamin C were also significantly lowered on alcohol supplementation. Treatment with Cassia auriculata leaf extract at a dose of 250 mg kg(-1) body weight and 500 mg kg(-1) body weight to rats administered alcohol, lowered the levels of TBARS and hydroperoxides and elevated the activities of SOD and CAT and the levels of reduced GSH in the liver, brain, kidney and intestine significantly compared to unsupplemented alcohol treated rats. Cassia auriculata leaf extract treatment restored the serum vitamin E, and vitamin C levels also to near those of the experimental control animals. Our data indicate that supplementation with Cassia auriculata leaf extract can offer protection against free radical mediated oxidative stress in experimental hepatotoxicity. In addition, histopathological studies of the liver and brain confirmed the beneficial role of Cassia auriculata leaf extract.     

Protective effect of ursolic acid on ethanol-mediated experimental liver damage in rats

Ursolic acid is a triterpenoid that exists in nature and is the major component of some traditional medicinal herbs. In this study, ursolic acid has been evaluated for its hepatoprotective effect against chronic ethanol-mediated toxicity in rats. Ethanol administration (7.9 g/kg/day) for 60 days resulted in increased oxidative stress, decreased antioxidant defense and liver injury. It also negatively affected the serum total protein, albumin and A/G ratio. Subsequent to the experimental induction of toxicity (i.e. after the initial period of 30 days) ursolic acid treatment performed by co-administering ursolic acid (10, 20 and 40 mg/kg body weight) for 30 days along with the daily dose of ethanol. While this treatment causing a significant improvement in body weight, food intake and serum protein levels, it decreases serum aminotransferase activities (aspartate aminotransferase and alanine aminotransferase) and total bilirubin levels. Ursolic acid improved the antioxidant status of alcoholic rats, which is evaluated by the decreased levels of lipid peroxidation markers in plasma (thiobarbituric acid reactive substances and lipid hydroperoxides) and increased levels of circulatory antioxidants such as reduced glutathione, ascorbic acid and alpha-tocopherol. Histopathological observations were also in correlation with the biochemical parameters. The activity of ursolic acid (20 mg/kg) compares well with silymarin, a known hepatoprotective drug, and seems to be better in certain parameters. The protective effect of ursolic acid is probably related to its antioxidant activities.     

Effects of vagotomy on circulating levels of catecholamines and corticosterone in the pigeon

The effects of bilateral cervical vagotomy on the blood levels of corticosterone, and catecholamines, adrenaline (A) and noradrenaline (NA), in pigeons, were studied. Plasma levels of corticosterone and NA were found to be significantly higher and of A lower, in the vagotomized (VgX) pigeons as compared to their sham-operated (VgS) controls. These changes in VgX pigeons are explained as caused mainly by the lack of the vagal tone.     

Suppression of sympathetic nervous system by short photoperiod and melatonin in the Syrian hamster

Exposure to short photoperiod or melatonin treatment brings about gonadal regression in Syrian hamsters. The possible influence of these treatments on the sympathetic nervous system (SNS) in these animals was investigated. Male Syrian hamsters were exposed to either long or short photoperiod or subjected to administration of melatonin or its vehicle solution. Exposure of hamsters to 10 weeks of short photoperiod, significantly reduced the noradrenaline (NA) turnover in the heart. Daily administration of melatonin for 8 weeks also resulted in a similar suppression of NA turnover in the heart. Hamsters that were treated with melatonin maintained a lowered metabolic rate as well, at and below thermoneutral temperature. These findings suggest that in a deep hibernator, short photoperiod could suppress the peripheral sympathetic activity and that melatonin may act as the endogenous mediator.     

Incorporation of32P-orthophosphate into phospholipids by a toxigenic and a nontoxigenic strain of Aspergillus flavus

The incorporation of³²P-orthophosphate into phospholipids by a toxigenic and a nontoxigenic strain ofAspergillus flavus was compared on a glucose-salts medium (AM medium) and a sucrose-yeast extract medium (YES medium). AM medium gave higher incorporation of³²P than YES medium. In AM medium the highest specific activities were found in phosphatidyl choline and phosphatidyl ethanolamine but in YES medium phosphatidyl inositol and phosphatidyl serine also had specific activities of the same order as phosphatidyl choline and phosphatidyl ethanolamine. Mycelia of the toxigenic strain grown and resuspended in AM medium yielded 1.4 times specific activities given by nontoxigenic strain. The two strains did not differ very much in the incorporation obtained in the other media combination tried. These results are in contrast to the large differences obtained in the incorporation of¹⁴C-acetate in earlier studies. The significance of these findings are discussed.These results were presented at the Symposium on the Chemistry and Metabolism of Lipids and Related Subjects held at Vallabhbhai Patel Chest Institute, Delhi on October 3–5, 1969.     

Effect of central cholinergic blockade on the hyperthermia evoked by prostaglandin E1 injected into the rostral hypothalamus of the rat.

The possibility of a cholinergic involvement in the hyperthermic action produced by the injection of prostaglandin E1 (PGE1) into the anterior hypothalamic/preoptic region of the rat brain was examined. Intracerebral injection of either atropine or mecamylamine prior to the injection of PGE1 failed to attenuate the PGE1-induced hyperthermia. Both atropine and mecamylamine by themselves produced a rise in colonic temperature. It thus seems unlikely that PGE1 evokes hyperthermia in the rat by releasing endogenous acetylcholine at muscarinic or nicotinic synapses in the rostral hypothalamus. The possibility that PGE1 acts by inhibiting the release of acetylcholine within this region requires additional investigation.     

Improved method for the analysis of furosemide in plasma by high-performance liquid chromatography

Modifications of existing rapid high-performance liquid chromatographic procedures for the determination of furosemide in plasma were made in order to achieve greater sensitivity. To a small volume of plasma was added an internal standard structurally related to furosemide. Then, following previously described procedures, acetonitrile was added to precipitate the proteins and the clear supernatant was separated. However prior to injection of the supernatant the pH and composition of the sample were adjusted. This modification of the sample enabled an injection volume of up to 300 μl of the supernatant to be injected onto the chromatographic column. The effluent was monitored spectrofluorimetrically. A standard linear calibration curve with a mean precision of ± 4.4% was obtained for plasma samples containing 20–900 ng/ml of furosemide. Two structurally related compounds were used as internal standards in the furosemide assay.     

Regulation of phospholipase D by tyrosine kinases

Activation of phospholipase D (PLD) represents part of an important signalling pathway in mammalian cells, Phospholipase D catalyzed hydrolysis of phospholipids generates phosphatidic acid (PA) which is subsequently metabolized to lyso-PA (LPA) or diacylglycerol (DAG). While DAG is an endogenous activator of protein kinase C (PKC), PA and LPA have been recognized as second messengers as well, Activation of PLD in response to an external stimulus may involve PKC, Ca²⁺, G-proteins and/or tyrosine kinases. In this review, we will address the role of protein tyrosine phosphorylation in growth factor-, agonist- and oxidant-mediated activation of PLD. Furthermore, a possible link between PKC, Ca²⁺, G-proteins and tyrosine kinases is discussed to indicate the complexity involved in the regulation of PLD in mammalian cells.     

Changes in expression of angiotensin receptor subtypes in the rat aorta during development

Quantitative autoradiography was used to characterize angiotensin AT1 and AT2 receptors, in the rat aorta at three developmental ages; embryonic day 18 (E18), and postnatal weeks 2 and 8. The expression of angiotensin receptors was higher in the aorta of E18 and 2-week-old rat. A major proportion of the angiotensin receptors expressed in the aorta at these two ages was AT2 (84 and 81% respectively). Conversely, in the aorta of 8-week-old rats, AT1 was the predominant angiotensin receptor subtype (71%). In 8-week-old rats, the AT2 subtype was also present (28%). In pre- and postnatal rats, [125I]Sar1-angiotensin II binding to AT1 receptors was sensitive to GTP gamma S whereas binding to AT2 receptors was not. AT2 receptors may serve an important role during stages of rapid growth of the aorta, and also have a significant function in the adult vasculature.