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Possible Protective Effects (possible + protective_effects)
Selected AbstractsMethimazole protects lungs during hepatic ischemia,reperfusion injury in rats: An effect not induced by hypothyroidismJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2007Tanju Tütüncü Abstract Background:, Hepatic ischemia,reperfusion injury may lead to remote organ failure with mortal respiratory dysfunction. The aim of the present study was to analyze the possible protective effects of methimazole on lungs after hepatic ischemia,reperfusion injury. Methods:, Forty male Wistar albino rats were randomized into five groups: a control group, in which bilateral pulmonary lobectomy was done; a hepatic ischemia,reperfusion group, in which bilateral pulmonary lobectomy was done after hepatic ischemia,reperfusion; a thyroidectomy,ischemia,reperfusion group (total thyroidectomy followed by, 7 days later, bilateral pulmonary lobectomy after hepatic ischemia,reperfusion); a methimazole,ischemia,reperfusion group (following methimazole administration for 7 days, bilateral pulmonary lobectomy was done after hepatic ischemia,reperfusion); and a methimazole +l -thyroxine,ischemia,reperfusion group (following methimazole and l -thyroxine administration for 7 days, bilateral pulmonary lobectomy was performed after hepatic ischemia,reperfusion). Pulmonary tissue specimens were evaluated histopathologically and for myeloperoxidase and malondialdehyde levels. Results:, All of the ischemia,reperfusion intervention groups had higher pulmonary injury scoring indices than the control group (P < 0.001). Pulmonary injury index of the ischemia,reperfusion group was higher than that of both the methimazole-supplemented hypothyroid and euthyroid groups (P = 0028; P = 0,038, respectively) and was similar to that of the thyroidectomized group. Pulmonary tissue myeloperoxidase and malondialdehyde levels in the ischemia,reperfusion group were similar with that in the thyroidectomized rats but were significantly higher than that in the control, and both the methimazole-supplemented hypothyroid and euthyroid groups. Conclusion:, Methimazole exerts a protective role on lungs during hepatic ischemia,reperfusion injury, which can be attributed to its anti-inflammatory and anti-oxidant effects rather than hypothyroidism alone. [source] Chronic lithium administration to FTDP-17 tau and GSK-3, overexpressing mice prevents tau hyperphosphorylation and neurofibrillary tangle formation, but pre-formed neurofibrillary tangles do not revertJOURNAL OF NEUROCHEMISTRY, Issue 6 2006Tobias Engel Abstract Glycogen synthase kinase-3 (GSK-3) has been proposed as the main kinase able to aberrantly phosphorylate tau in Alzheimer's disease (AD) and related tauopathies, raising the possibility of designing novel therapeutic interventions for AD based on GSK-3 inhibition. Lithium, a widely used drug for affective disorders, inhibits GSK-3 at therapeutically relevant concentrations. Therefore, it was of great interest to test the possible protective effects of lithium in an AD animal model based on GSK-3 overexpression. We had previously generated a double transgenic model, overexpressing GSK-3, in a conditional manner, using the Tet-off system and tau protein carrying a triple FTDP-17 (frontotemporal dementia and parkinsonism linked to chromosome 17) mutation. This transgenic line shows tau hyperphosphorylation in hippocampal neurones accompanied by neurofibrillary tangles (NFTs). We used this transgenic model to address two issues: first, whether chronic lithium treatment is able to prevent the formation of aberrant tau aggregates that result from the overexpression of FTDP-17 tau and GSK-3,; second, whether lithium is able to change back already formed NFTs in aged animals. Our data suggest that progression of the tauopathy can be prevented by administration of lithium when the first signs of neuropathology appear. Furthermore, it is still possible to partially reverse tau pathology in advanced stages of the disease, although NFT-like structures cannot be changed. The same results were obtained after shut-down of GSK-3, overexpression, supporting the possibility that GSK-3 inhibition is not sufficient to reverse NFT-like aggregates. [source] Zearalenone induces immunotoxicity in mice: possible protective effects of radish extract (Raphanus sativus)JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 6 2008Jalila Ben Salah-Abbès Radish (Raphanus sativus) has been extensively studied for its preventive effects against different degenerative diseases. Zearalenone (ZEN) is a mycotoxin produced by Fusarium spp and is frequently implicated in immunological disorders and occasionally in hyperoestrogenic syndromes contributing to the increased risk of cancer and other diseases. The aims of this study were, firstly, to quantitatively evaluate the Tunisian radish extract (TRE) for its total flavonoids, isothiocyanates and antioxidant activity and, secondly, to investigate the protective role of TRE against immune system disorders in Balb/c mice treated with ZEN for two weeks. The results indicated that mice treated with ZEN (40 mg kg,1) alone showed a significant decrease in lymphocytes of the total white blood cells, immunoglobulin profile (IgG and IgM), B cells, T-cell sub-types (CD3+, CD4+ and CD8+) and natural killer and pro-inflammatory cytokines. Mice treated with TRE (5, 10 or 15 mg kg,1) for 7 days before, during or after ZEN treatment, however, showed a significant improvement in lymphocyte, immunoglobulin profile, T-cell sub-types, B cells and pro-inflammatory cytokines. Moreover, treatment with the highest dose of TRE (15 mgkg,1) enhanced the release of tumour necrosis factor-, and interleukin-1, but the other parameters were comparable with those of the control. It could be concluded that TRE was effective in protecting against ZEN-induced immunological disorders. These results supported our hypothesis that TRE contains several compounds that are able to prevent or inhibit ZEN toxicity. [source] Cover Picture , Mol.MOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 2 2008Nutr. Used to flameproof electronic equipment, brominated flame retardants (BFRs) also escape into the environment where they accumulate in organisms. Although consumption of fatty fish is recommended because of the healthy effects of the omega-3 fatty acids, there has been little information on the possible protective effects of the omega-3 fatty acids in relation to contaminants. This Special Issue of Molecular Nutrition & Food Research gives an up-to-date overview of the current state of the science dealing with the occurrence and possible health effects of BFRs in food. [source] Reduction of carbon tetrachloride-induced nephropathy by melatonin administrationCELL BIOCHEMISTRY AND FUNCTION, Issue 2 2005Murat Ogeturk Abstract The aim of this study was to investigate possible protective effects of melatonin on carbon tetrachloride (CCl4)-induced renal damage in rats. A total of 24 animals were divided into three equal groups: the control rats received pure olive oil subcutaneously, rats in the second group were injected with CCl4 (0.5,ml,kg,1, s.c. in olive oil) and rats in the third group were injected with CCl4 (0.5,ml,kg,1) plus melatonin (25,mg,kg,1, s.c. in 10% ethanol) every other day for 1 month. At the end of the experimental period, the animals were sacrificed and blood samples were collected. The kidneys were removed and weighed. Urea and creatinine levels were determined in blood samples. Histopathological examination of the kidney was performed using light microscopic methods. Administration of CCl4 significantly increased relative kidney weight (g,per,100,g body weight) and decreased serum urea levels compared to controls (p,<,0.01). Melatonin treatment significantly (p,<,0.01) reduced relative kidney weight, and it produced a statistically equal (p,=,0.268) relative weight with the kidneys of control rats. CCl4 administration alone also caused histopathologically prominent damage in the kidney compared to the control group. Glomerular and tubular degeneration, interstitial mononuclear cell infiltration and fibrosis, vascular congestion around the tubules, and interstitial haemorrhage in perivascular areas were observed in the renal cortex and cortico-medullary border. However, the affect of CCl4 on the medulla was limited. Melatonin provided protection against CCl4 -induced renal toxicity as was evident by histopathological evaluation. In view of the present findings, it is suggested that melatonin protects kidneys against CCl4 toxicity. Copyright © 2004 John Wiley & Sons, Ltd. [source] Coenzyme Q10 prevents human lens epithelial cells from light-induced apoptotic cell death by reducing oxidative stress and stabilizing BAX,/,Bcl-2 ratioACTA OPHTHALMOLOGICA, Issue 3 2010Marcus Kernt Abstract. Background:, Cataract is one of the most prevalent eye disease and a major cause for legal blindness in the world. Beside others, cumulative light-exposure and apoptotic cell death are significantly associated with cataract development. In contrast, supplementation with antioxidants has been suggested to prevent premature cataractogenesis. This study investigates possible protective effects of Coenzyme Q10 (CoQ10) regarding light-induced stress and apoptotic cell death in human lens epithelial cells (LEC). Methods:, Human LEC were either pre-incubated with CoQ10 or not and then exposed to white light. After 10,40 min of irradiation viability, induction of intracellular reactive oxygen species (ROS), apoptosis and cell death was determined. Expression of apoptotic BAX and anti-apoptotic Bcl-2 protein and their mRNA were determined by RT-PCR and Western blot analysis. Results:, Light exposure decreased LEC viability and Bcl-2 expression and increased intracellular ROS, apoptotic cell death, and BAX expression in a time-of-irradiation-dependent manner. Phototoxic cell death and apoptosis, as well as decrease of Bcl-2 and increase in BAX expression was significantly reduced, when cells were pre-incubated with CoQ10. Conclusions:, In this study, CoQ10 significantly reduced light-induced LEC-damage and attenuated phototoxic effects on BAX and Bcl-2 expression. Therefore, CoQ10 supplementation might also be useful in preventing LEC death and consecutive cataract formation in vivo. 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