26 research outputs found
URB597, an Inhibitor of Fatty Acid Amide Hydrolase, Reduces Chemical Neuropathy in Diabetic Rats
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Glabridin as a major active isoflavan from<i>Glycyrrhiza glabra</i>(licorice) reverses learning and memory deficits in diabetic rats
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Effects of rosmarinic acid on acetaminophen-induced hepatotoxicity in male Wistar rats
No full textContext: Drug-induced liver injury is a significant worldwide clinical problem. Rosmarinic acid (RA), a natural phenol, has antioxidant effects. Objective: The effects of RA against acetaminophen (N-acetyl-p-amino-phenol (APAP))-induced oxidative damage and hepatotoxicity in rats were investigated. Materials and methods: Male Wistar rats were pretreated with RA (10, 50 and 100 mg/kg, i.g.) for one week. On day 7, rats received APAP (500 mg/kg, i.p.). Then aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin, total protein, malondialdehyde (MDA), glutathione (GSH), total antioxidant capacity (TAC), glutathione S-transferase (GST), cytochrome CYP450 and histopathological changes were determined. Results: APAP-induced oxidative stress in liver by a significant increase in the level of MDA (7.6 ± 0.21 nmol/mg) as well as a decrease in the contents of TAC (1.75 ± 0.14 μmol/g), GSH (1.9 ± 0.22 μmol/g) and GST) 3.2 ± 0.28 U/mg). RA treatment decreased MDA (4.32 ± 0.35 nmol/mg) but increased the contents of TAC (3.51 ± 0.34 μmol/g), GSH (3.42 ± 0.16 μmol/g) and GST (5.71 ± 0.71 μmol/g) in APAP group. RA 100 mg/kg decreased ALT (91.5 ± 1.5 U/L), AST (169 ± 8.8 U/L) and CYP450 (3 ± 0.2 nmol/min/mg) in APAP group. Histologically RA attenuated hepatic damage by decreasing necrosis, inflammation, and haemorrhage in liver sections of APAP group. Discussion and conclusions: This is the first report that oral administration of RA dose-dependently elicited significant hepatoprotective effects in rats through inhibition of hepatic CYP2E1 activity and lipid peroxidation. RA-protected hepatic GSH and GST reserves and total tissue antioxidant capacity
Chelating effects of carnosine in ameliorating nickel-induced nephrotoxicity in rats
No full text The kidney is one of the main organs affected by nickel toxicity. We investigated the protective effects of carnosine on nickel-induced oxidative stress in kidney of rats. Animals received NiSO4 (20 mg·kg−1·day−1 intragastrically) and (or) carnosine (10 mg·kg−1·day−1 intragastrically) for 21 days and then were evaluated for biochemical, molecular, and histopathological alterations. Nickel caused an increase in renal levels of malondialdehyde and a decrease in reduced glutathione, catalase, and superoxide dismutase levels and total antioxidant capacity. Carnosine prevented the prooxidant and antioxidant imbalance induced by nickel. Nickel-treated rats showed an increase in serum creatinine, urea, and uric acid with a concomitant decrease in albumin. Nickel markedly accumulated in kidney of exposed rats, but its concentration was effectively reduced by carnosine treatment. Carnosine corrected the biochemical abnormalities and the elevated renal TNF-α and IL-6 levels in the nickel-treated group. It also attenuated nickel-induced abnormalities in renal architecture. Although carnosine showed antioxidant and anti-inflammatory effects in renal tissue of nickel-exposed rats, we cannot clearly attribute the protective effect of carnosine to these effects. Instead, the beneficial effect of carnosine observed in the current study may be due to chelation between nickel and carnosine. Thus, carnosine may represent a therapeutic option to protect against nickel-induced nephrotoxicity that deserves further consideration and examination. </jats:p
Beneficial effects of rosmarinic acid against alcohol-induced hepatotoxicity in rats
No full text Alcohol is a severe hepatotoxicant that causes a variety of liver disorders. Rosmarinic acid (RA), a natural phenol, shows some biological activities, including antioxidant and anti-inflammatory effects. We investigated the effects of RA (10 mg/kg) against ethanol-induced oxidative damage and hepatotoxicity in rats. Animals received ethanol (4 g/kg, i.g.) and (or) RA (10 mg/kg, i.g.) daily for 4 weeks. At the end of the treatment period, rats were weighed and use for biochemical, molecular, and histopathological examinations. Ethanol increased hepatic lipid peroxidation (P < 0.001) and decreased hepatic levels of reduced glutathione (P < 0.01), catalase (P < 0.05), and superoxide dismutase (P < 0.001) compared with control group. RA prevented the prooxidant and antioxidant imbalance induced by ethanol in liver. Furthermore, RA ameliorated the increased liver mass, serum levels of ALT, AST, LDH, TNF-α, and IL-6 in ethanol group. Necrosis and infiltration of inflammatory cells in liver parenchyma were attenuated by RA treatment. Our findings showed that RA prevents ethanol-induced oxidant/antioxidant imbalance and liver injury in an experimental model of ethanol-induced hepatotoxicity. Therefore, RA may be a good candidate to protect against ethanol-induced hepatotoxicity; this deserves consideration and further examination. </jats:p
Effects of Hypericum perforatum extract on diabetes-induced learning and memory impairment in rats
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