排序方式: 共有224条查询结果,搜索用时 31 毫秒
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Ahmet Yesildağ Ahmet Özden H. Ramazan Yılmaz Efkan Uz Yetkin Ağackıran Mihrican Yesildağ Nigar Yılmaz Rana Sırmalı Hüseyin Vural Mustafa Nazıroğlu 《Cell biochemistry and function》2009,27(3):142-147
It has been suggested that reactive oxygen species (ROS) plays an important role in radio contrast media (RCM)‐induced ischemia reperfusion tissue injury although antioxidants may have protective effects on the injury. We investigated the effects of erdosteine as an antioxidant agent on RCM‐induced liver toxicity in rats by evaluation of lipid peroxidation (as TBARS), catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and glutathione peroxidase (GSH‐Px) values and histological evaluation. Twenty‐one rats were equally divided into three groups as follows: control, RCM, and RCM plus erdosteine. RCM was intraperitoneally administered for 1 day. Erdosteine was administered orally for 2 days after RCM administration. Liver samples were taken from the rats and they homogenized in a motor‐driven tissue homogenizer. TBARS levels were significantly (p < 0.005) higher in RCM group than in control although SOD activities significantly (p < 0.05) decreased in RCM group. TBARS levels were lower in RCM plus erdosteine group than in control although SOD activity and GSH level increased (p < 0.05) in liver as compared to RCM alone. Erdosteine showed also histopathological protection (p < 0.0001) against RCM induced hepatotoxicity. GSH‐Px and CAT activities were not statistically changed by the erdosteine. According to our results, it can be concluded that radiocontrast media can induce oxidative stress in liver as suggested by previous studies. Erdosteine seems to be protective agent on the radiocontrast media‐induced liver toxicity by inhibiting the production of ROS via the enzymatic antioxidant system. Copyright © 2009 John Wiley & Sons, Ltd. 相似文献
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Familial Mediterranean fever (FMF) is a genetic disorder with acute inflammatory serosal attacks due to MEFV gene mutations
which resides in chromosome 16. Lack of a C5a inhibitor activity in the peritoneum has previously been proposed in part to
contribute in propagation of the serosal inflammation in FMF attacks. The aim of this study is to investigate C5a receptor
(C5aR) gene polymorphism in patients with FMF and its relation to the main features of the disease. A polymorphism in the
coding region of C5aR gene leading to C to T transition at nucleotide position 450 has been investigated in 85 non-related
Turkish FMF patients and 160 non-related healthy controls by using PCR-RFLP. The frequencies of C5aR gene 450 CT genotype
and T allele were not significantly different between Turkish FMF patients and healthy subjects (14.12 and 8.24% for FMF vs.
10 and 5% for controls, respectively). C5aR gene 450 CT genotype tended to associate with the presence Henoch-Schonlein purpura
(OR: 1.25, 95% CI: 0.917–1.704, P = 0.017) but with no other clinical findings of the disease. C5aR polymorphism might be searched in populations having high
prevalence of FMF. 相似文献
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Melek Bor-Kucukatay Suleyman Demir Ramazan Akbay Dursun Dursunoglu Beyza Akdag Ender Semiz 《Molecular biology reports》2010,37(1):171-178
This study aimed to investigate the relationship between endothelial nitric oxide synthase Glu(298)Asp gene polymorphism and hemorheological parameters. Red blood cell (RBC) deformability, aggregation were measured using an ectacytometry, whole blood, plasma viscosities were determined by a viscometer. Restriction fragment length polymorphism was used to detect polymorphism. Plasma nitrite, nitrate concentrations were determined by Griess method. The genotype distribution of the control group was as follows: 50 (67.5%) GG, 21 (28.4%) GT, 3 (4.1%) TT. A 48 (57.8%) of the patients with CAD had GG, 28 (33.7%) GT, 7 (8.5%) of them TT genotype. RBC aggregation index of CAD patients with G allele was higher and t½ lower compared to controls carrying the same allele. The amplitude of RBC aggregation of healthy subjects with T allele, who are under increased cardiovascular risk was lower compared to control subjects with G allele. The results of this study indicate that, alterations in RBC aggregation seem to be a consequence of CAD, more than being a preexisting cause. Additionally, some compensatory mechanisms by causing decrements in RBC aggregation, may help regulation of circulation in healthy individuals with high cardiovascular risk. 相似文献
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Protective Effects of Caffeic Acid Phenethyl Ester on Cyclophosphamide‐Induced Hemorrhagic Cystitis in Rats 下载免费PDF全文
Ersin Uysal H. Ramazan Yılmaz Yunus Ugan Atila Altuntas Atalay Dogru Ali Kutlucan Sevket Ercan Tunc 《Journal of biochemical and molecular toxicology》2015,29(12):559-563
We investigated the protective effect of caffeic acid phenethyl ester (CAPE) on cyclophosphamide‐induced hemorrhagic cystitis in rats in comparison with 2‐mercaptoethane sulfonate (MESNA). Forty male rats were randomized into four groups: group 1 (control), group 2 (cyclophosphamide), group 3 (cyclophosphamide + MESNA), group 4 (cyclophosphamide + CAPE). Cyclophosphamide injection increased malondialdehyde levels indicating oxidative stress, whereas CAPE and MESNA ameliorated malondialdehyde levels in the bladder (p < 0.05). Only catalase activities were decreased significantly in both groups (cyclophosphamide + MESNA and cyclophosphamide + CAPE, p < 0.05). Pretreatment with CAPE (p < 0.01) resulted in a significant decrease in nitric oxide levels when compared with the cyclophosphamide group. When we consider the studies that show the critical importance of increased nitric oxide levels in pathogenesis of cyclophosphamide‐induced hemorrhagic cystitis, we suggest that it would be more beneficial to use MESNA with CAPE to prevent histological damage. 相似文献
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Protective agent, erdosteine, against cisplatin-induced hepatic oxidant injury in rats 总被引:5,自引:0,他引:5
Cisplatin, one of the most active cytotoxic agents against cancer, has several toxicities. Hepatotoxicity is one of them occurred
during high doses treatment. The aim of this study was to determine the effects of erdosteine against cisplatin-induced liver
injury through tissue oxidant/antioxidant parameters and light microscopic evaluation. The rats were randomly divided into
three groups: control (n=5), cisplatin (10 mg/kg, n=6) and cisplatin+erdosteine (50 mg/kg/day oral erdosteine, n=8) groups. The rats were sacrificed at the 5th day of cisplatin treatment. The liver tissues were examined with light microscopy
and oxidant/antioxidant biochemical parameters. The malondialdehyde (MDA) and nitric oxide (NO) levels were increased in the
cisplatin group in comparison with the control and cisplatin+erdosteine groups (p<0.05). There was no significant difference in MDA and NO levels between control and cisplatin+erdosteine groups. The activities
of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were higher in cisplatin+erdosteine group
than cisplatin group (p<0.05). However, the CAT and GSH-Px activities were significantly lower in cisplatin group than in control group (p<0.05). The light microscopic examination revealed that cytoplasmic changes especially around cells of central vein were observed
in cisplatin group. Hepatocellular vacuolization was seen in these cells. In the cisplatin plus erdosteine group, a decrease
in cytoplasmic changes with the hepatocytes and sinusoidal dilatations around cells of central vein were noticed in as compared
to cisplatin group. In the light of microscopic and biochemical results, it was concluded that cisplatin-induced liver damage
in high dose and erdosteine prevented this toxic side effect by the way of its antioxidant and radical scavenging effects.
(Mol Cell Biochem 278: 79–84, 2005) 相似文献
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Cicek E Sutcu R Gokalp O Yilmaz HR Ozer MK Uz E Ozcelik N Delibas N 《Molecular and cellular biochemistry》2005,277(1-2):131-135
Isoniazid (INH) has neurotoxic effects such as seizure, poor concentration, subtle reduction in memory, anxiety, depression and psychosis. INH-induced toxic effects are thought to be through increased oxidative stress, and these effects have been shown to be prevented by antioxidant therapies in various organs. Increased oxidative stress may be playing a role in these neurotoxic effects. N-methyl D-aspartat receptors (NMDA) are a member of the ionotropic group of glutamate receptors. These receptors are involved in a wide variety of processes in the central nervous system including synaptogenesis, synaptic plasticity, memory and learning. Erdosteine is a potent antioxidant and mucolytic agent. We aimed to investigate adverse effects of INH on rat hippocampal NMDAR receptors, and to elucidate whether erdosteine prevents possible adverse effects of INH. In the present study, compared to control group, NMDAR2A (NR2A) receptors were significantly decreased and malondialdehyde (MDA), end product of lipid peroxidation, production was significantly increased in INH-treated group. On the other hand, administration of erdosteine to INH-treated group significantly increased NR2A receptors and decreased MDA production. In conclusion, decreasing NR2A receptors in hippocampus and increasing lipid peroxidation correlates with the degree of oxidative effects of INH and erdosteine protects above effect of INH on NR2A receptors and membrane damage due to lipid peroxidation by its antioxidant properties. 相似文献
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Demir R Acar G Tanriover G Seval Y Kayisli UA Agar A 《Folia histochemica et cytobiologica / Polish Academy of Sciences, Polish Histochemical and Cytochemical Society》2005,43(3):143-150
The aim of this study was to investigate whether excess of vitamin B6 leads to ultrastructural changes in cerebral cortex of forty-eight healthy albino rats which were included in the study. Saline solution was injected to to the control groups (CG-10, n = 12 for 10 days; CG-15, n = 12 for 15 days; CG-20, n=12 for 20 days). The three experimental groups (EG-10, n = 12; EG-15, n = 12; EG-20, n = 12) were treated with 5 mg/kg vitamin B6 daily for 10 days (EG-10), 15 days (EG-15) and 20 days (EG-20). Brain tissues were prepared by glutaraldehyde-osmium tetroxide double fixation for ultrastructural analysis. No significant changes were observed in the control groups. The ultrastructural analysis revealed that the numbers of damaged mitochondria, lipofuscin granules and vacuoles were significantly higher in all the experimental groups than in the control groups (p < 0.05). However, synaptic density was significantly decreased in the experimental groups as compared to the control groups (p < 0.05). The results suggest that the excess of vitamin B6 intake causes damage to the cerebral cortex due to cellular intoxication and decreased synaptic density. Thus, careful attention should be paid to the time and dose of vitamin B6 recommended for patients who are supplemented with this vitamin. 相似文献