Search

AIM: The present study explored Cynodon dactylon hydro-ethanolic extract (CDE) effect on scopolamine-induced amnesic rats. MATERIALS AND METHODS: C. dactylon extract was subjected to antioxidant (DPPH and H2O2) and acetylcholinesterase enzyme tests by in vitro methods. Scopolamine (1 mg/kg, i.p) was administered to rats except for normal control. Donepezil (3 mg/kg, p.o), CDE (100, 200, and 400 mg/kg p.o) were administered to treatment groups. Behavioral paradigm: Morris water maze (MWM), elevated plus maze (EPM), and passive avoidance test (PAT) were conducted. Later, rats were sacrificed and brain homogenate was tested for levels of acetylcholinesterase, glutathione, and lipid peroxidase. Histopathology examination of cortex and hippocampus of all the groups was done. STATISTICAL METHOD: The statistical methods used were ANOVA and Tukey's post hoc test. RESULTS: CDE antioxidant activity was demonstrated by decreasing DPPH and H2O2 levels confirmed through in vitro analysis. Treatment group rats reversed scopolamine induced amnesia by improvement in spatial memory, decreased transfer latency and increased step through latency significantly (P<0.001) in behavior models such as morris water maze, elevated plus maze and passive avoidance task respectively. CDE modulated acetylcholine transmission by decreased acetylcholinesterase enzyme level (P < 0.001) and scavenging scopolamine-induced oxidative stress by increased reduced glutathione levels and decreased lipid peroxidation levels in the rat brain. CDE and donepezil-treated rats showed mild neurodegeneration in comparison to scopolamine-induced severe neuronal damage on histopathology examination. CONCLUSION: C. dactylon extract provides evidence of anti-amnesic activity by the mechanism of decreased acetylcholinesterase enzyme level and increased antioxidant levels in scopolamine-induced amnesia in rats. [ABSTRACT FROM AUTHOR]

Objectives: To determine the effects of ß-adrenoceptor and muscarinic agonists on the contractile rate of isolated right atria of rats fed a high fructose diet with or without rosiglitazone (RSG). Materials and Methods: Male Sprague Dawley rats were assigned to four groups and given ad libitum access to one of the following diets: standard chow, standard chow supplemented with 4 mg/kg/day RSG, a high fructose diet and a high fructose diet with 4 mg/kg/day RSG. All the groups were maintained on these regimens for three weeks with weekly measurements of systolic blood pressure and body weight. At the end of the three weeks, the rats were exsanguinated and the hearts were rapidly removed following which blood glucose, insulin and lipid profiles were estimated. The right atria were isolated from the heart and their responsiveness to sympathetic and parasympathetic agonists was studied. Results: Basal, spontaneous, isolated atrial pacemaker rate was diminished in fructose-fed rats. The maximum pacemaker rate to isoproterenol or norepinephrine was unchanged in fructose-fed rats. Further, the increase in atrial rate and half maximal effective concentration values for each agent were also unaffected. The sensitivity to negative chronotropic action of acetylcholine was enhanced in fructose fed rats, whereas the response to carbachol was unchanged. The increased sensitivity to acetylcholine was restored by RSG treatment. Conclusion: High fructose diet induced insulin resistance and hypertension with alterations in basal spontaneous pacemaker, enhanced sensitivity to cholinergic agonist without any changes in the response to adrenergic and cholinergic receptor activation. Treatment with insulin sensitizer rosiglitazone was able to prevent all these changes. The present study suggests that rosiglitazone may have effect on the cardiovascular system in addition to the insulin sensitising action. [ABSTRACT FROM AUTHOR]

Objectives: The aim of the present study was to investigate the involvement of nitric oxide in 5-HT3 receptor agonist-induced fluid accumulation in jejunum and colon of anesthetized rats. Materials and Methods: Fluid movement in jejunum and colon were determined simultaneously in the same rat, by modifying the Beubler method. Nω-nitro-L-arginine (L-NNA, 20 mg/kg, s.c) alone and in combination with L-arginine (L-Arg, 150 mg/kg s.c) or D-arginine (D-Arg, 150 mg/kg, s.c) were administered 30 min before administration of 1-PBG (18.5 μg/kg, i.v). Results: Intravenous administration of 1-phenylbiguanide (1-PBG) induced a net secretion of fluid in both jejunum and colon. 1-PBG had a more prominent secretory effect in the colon, causing a three-fold increase in volume of fluid secreted/g of colon than in the jejunum. Pretreatment with (L-NNA) prevented the 1-PBG-induced fluid accumulation in both jejunum and colon. The inhibitory effect of L-NNA on 1-PBG-induced fluid accumulation was reversed by L-Arg but not by D-Arg. Conclusion: These results provide evidence that nitric oxide plays an important role in 5-HT3 receptor agonist-induced fluid accumulation in jejunum and colon of anesthetized rats. [ABSTRACT FROM AUTHOR]