BACKGROUND: Methotrexate (MTX) is an anticancer drug. Many studies have reported that MTX causes oxidative stress-associated damage in the small intestine. The purpose of this study was to investigate the possible protective effect of resveratrol (RES), an antioxidant, against MTX-induced damage in the small intestine. MATERIALS AND METHODS: Twenty-four Spraque Dawley rats were randomly divided into four groups; the control group, the RES group given 20 mg/kg RES for 10 days, the MTX group given single dose 30 mg/kg MTX, MTX+RES group given 20 mg/kg RES i.p. for 7 days and 30 mg/ kg MTX i.p. on the 7th day, RES being maintained for 3 further days. All rats were sacrifi ced on the 10th day, and small intestinal tissue was removed for histopathological and biochemical analysis. Additionally, mucosal apoptosis was analyzed using the TUNEL method. RESULTS: Histopathologically, villar fusion, atrophic villus epithelium, cystic expansion in crypts, hemorrhage and infl ammatory cell infi ltration were seen in the small intestine in the MTX group. In the MTX+RES group this histopathological damage decreased signifi cantly. Apoptotic score was signifi cantly higher in the MTX group and signifi cantly lower in the MTX+RES group. Tissue malondialdehyde (MDA) level was signifi cantly higher in the MTX group. Superoxide dismutase (SOD) activity was signifi cantly decreased in the MTX group. The MDA level in the MTX+RES group decreased while SOD and catalase (CAT) activities rose, this was not statistically signifi cant. CONCLUSİONS: RES treatment may ameliorate MTX induced small intestine damage especially at histopathological level (Tab. 2, Fig. 2, Ref. 41).
Purpose: To investigate the healing effect of resveratrol on ischemia, inflammation and oxidative injury in brain and heart tissue of rats in an experimentally induced carbonmonoxide (CO) intoxication model. Methods: Twenty-eight mature female Spraque Dawley rats were randomized into four groups of seven animals each. Groups I and II inhaled room air for 60 minutes. Groups III and IV inhaled a high concentration of a 5000 ppm CO gas mixture at 4 L/min until loss of consciousness. Blood CO levels were measured from 1 mL blood specimens collected from the tail vein. Groups I and III received 1 mL of normal saline while groups II and IV received 25 mg/kg resveratrol intraperitoneally. At the end of 48 hour, the rats were sacrified and later blood, brain and heart tissue samples were taken for histopathological and biochemical evaluation. Neuron damage scores, percentages of degenerate neurons and apoptosis rates in the cortex and hypothalamus were calculated in brain tissues. Myocyte degeneration, vascular congestion and myocyte apoptosis rates were calculated in heart tissues. Total antioxidant (TAS), total oxidant (TOS) and oxidative stress index (OSI) levels were also calculated from the tissue samples.Results: Histopathological evaluation revealed that resveratrol significantly reduced tissue damage in the brain when groups III and IV were compared (p<0.05). Resveratrol also reduced cardiac myocyte degeneration and myocyte apoptosis rate in heart tissue (p=0.004 and p=0.002). No positive effect was determined at analysis of antioxidant parameters. Conclusion:The results of this study investigated that resveratrol administration in experimental setting may be beneficial in healing injury secondary to CO intoxication in brain and heart tissue.
Carbon monoxide (CO) is a colorless, odorless, tasteless, nonirritating gas which normally presents at a level of 0.001% in the atmosphere. It emerges when carbon-based compounds used as fuels for cooking and heating are incompletely consumed, or during fires (1). CO is one of the most important global agents in injury-and intoxication-related mortality (2). Children and the elderly are more rapidly affected. Other factors increasing disposition are exercise, stress, and anemia. High atmospheric concentrations and long-term exposure are other important factors. Due to their high oxygen requirements, brain, heart, and liver are the most susceptible organs to the hypoxic effects of CO exposure (3). Studies have determined that the cardiac effect is associated with Abstract Aim: The purpose of this study was to investigate the protective effects of ethyl pyruvate (EP) and dimethyl sulfoxide (DMSO) on ischemic tissue in brain and cardiac and hepatic tissues in experimentally induced carbon monoxide (CO) intoxication.Material and Methods: Thirty-five mature female Sprague Dawley rats were randomized into five groups of seven animals each. Group 1 received no CO or treatment. Rats in groups 2, 3, 4 and 5 were made to inhale a high-concentration 5000 ppm CO gas mixture for 60 min at 4 L/min. CO levels were then measured from 1 mL tail vein blood. Group 2 received no therapeutic agent, group 3 received 6 mg/kg intraperitoneal (ip) DMSO, group 4 received 50 mg/kg ip EP, group 5 received 50 mg/kg EP and 6 mg/kg DMSO ip. All rats were sacrificed by decapitation. Brain, cardiac and hepatic tissues were removed and histopathological scores were compared. Results:Comparison of group 2 with group 3 and group 2 with group 5 revealed that DMSO alone and EP + DMSO exhibited a reducing effect on degree of cerebral neuronal alteration, degenerative neuron rates, and total cardiac injury score (p=0.005, p=0.002, p=0.004 and p=0.002, p=0.001, p=0.004 respectively). There was no histopathological difference between group 2 and group 4 suggesting EP alone had no therapeutic effect on histopathological injury. Conclusion:Based on our study findings, EP administered alone exhibited no protective effects on the organ injuries investigated, while DMSO exhibited reducing effects on degree of neuron alteration, rates of degenerative neurons, and total cardiac injury scores. An ameliorating effect on cardiac and hepatic injury was more prominent with combined treatment.
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