Biomedical subjects

Recep Sutcu

Publications and source records attributed to Recep Sutcu.

13 recordsLinked to original sources

PubMed2006

Melatonin increases NMDA receptor subunits 2A and 2B concentrations in rat hippocampus.

We investigated that the effects of melatonin on N-methyl-D: -aspartat receptor (NMDAR) subunits 2A and 2B concentrations and on markers of oxidative stress in hippocampus of rats treated with melatonin for 4 weeks. Animals were divided into four groups according to their melatonin doses (control group (C), n = 7; 5 mg/kg group (M5), n = 7; 10 mg/kg group (M10), n = 8; 20 mg/kg group (M20), n = 8) and received the melatonin as intraperitoneal injection. After 4 weeks of treatment, electrophoretic examination was done using sodium dodecyl sulfate/polyacrilamide gel electrophoresis (SDS-PAGE) and Western blotting in hippocampal homogenates of different groups. Malondialdehyde (MDA), an end product of lipid peroxidation, was assayed in all groups. There were significant increases in both NMDAR 2A; 5 mg/kg group (n = 3, p < 0.05), 10 mg/kg group (n = 3, p < 0.05), 20 mg/kg group (n = 3, p < 0.05) and NMDAR 2B expressions; 5 mg group (n = 3, p < 0.05), 10 mg group (n = 3, p < 0.05), 20 mg group (n = 3, p < 0.05), compared to the control group. No significant difference in MDA concentrations was found between groups. The present study clearly demonstrates that melatonin alters hippocampal NMDAR subunit concentrations in a dose-dependent manner without causing lipid peroxidation.

Animals↗

PubMed2006

Pentoxifylline, a methyl xanthine derivative, reduces peritoneal adhesions and increases peritoneal fibrinolysis in rats.

Peritoneum has an intrinsic fibrinolytic activity that breaks the peritoneal adhesions. Peritoneal injuries with ischemia interfere this fibrinolytic activity and cause adhesions. Pentoxifylline, a methyl xanthine derivative, improves blood flow by decreasing its viscosity and also increases fibrinolytic activity in plasma. We hypothesized that pentoxifylline would increase peritoneal fibrinolysis and ameliorate adhesions. A rat model of peritoneal adhesion (cecal abrasion with gauze, n = 15 for each group) was used to test this hypothesis and cardinal parameters of peritoneal fibrinolysis were measured in peritoneal samples. No medication was given in control animals, while pentoxifylline was administered intraperitonealy (IP) (25 mg/kg, before abdominal closure to whole abdomen) or intravenously (IV) (25 mg/kg, for 9 days after operation) in the experimental groups. At postoperative day 10, peritoneal biopsies were obtained and adhesions were graded qualitatively. Activities and concentrations of tissue plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), tPA/PAI-1 complex and hydroxyproline contents were determined. Total adhesion scores were decreased in both treated groups. Mean levels of tPA concentration and tPA activity were increased in the treated groups compared to controls (p < 0.001 and p = 0.001, respectively). The tPA/PAI-1 complex levels were similar among the three groups. PAI-1 levels were lower in animals receiving IP pentoxifylline compared to control animals and those treated with IV pentoxifylline (p = 0.048, p = 0.015, respectively). Peritoneal hydroxyproline levels were similar among the three groups. Our results suggest that pentoxifylline administration either through IV or IP may reduce peritoneal adhesion formation probably by altering peritoneal fibrinolytic activity.

Animals↗

PubMed2006

Asymmetric dimethylarginine and nitric oxide levels as signs of endothelial dysfunction in Behcet's disease.

Behcet's disease (BD) has been known for many years, yet the etiology of the systemic vasculitis remains unknown. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA is involved in endothelial dysfunction in various vascular diseases and its level in BD is unclear. This study was performed to evaluate the relationship between ADMA and NO levels in plasma of patients with BD. There were 3 groups of 30 subjects: (a) controls, (b) BD patients with mucocutaneous involvement, and (c) BD patients with vascular involvement. Plasma NO levels were assayed by spectrophotometry and plasma ADMA levels were assayed by an ELISA test. Plasma ADMA levels were higher in both groups of BD patients than in the controls; the ADMA levels were higher in the BD patients with vascular involvement than in the mucocutaneous group. Plasma NO levels were lower in both groups of BD patients than in controls; plasma NO levels were lower in the BD patients with vascular involvement than in mucocutaneous group. In the combined groups of 60 BD patients, there was significant inverse correlation between the plasma concentrations of ADMA and NO (r = -0.570, p <0.001). Plasma lipid profiles did not differ significantly between the BD patients and the controls. These results are evidence for increased plasma ADMA levels and decreased plasma NO levels as risk factors for cardiovascular events in BD patients. Inhibition of NO synthesis by ADMA may contribute to vascular involvement in BD.

Adult↗

PubMed2005

Does melatonin protect or treat brain damage from traumatic oxidative stress?

A variety of experimental studies have demonstrated the neuroprotective effects of melatonin, based on its antioxidant activity. In a prospective randomized study, the effects of melatonin were investigated in experimental head trauma-induced oxidative stress in rabbits. The experimental study was performed on 30 rabbits. The animals were divided into three groups. Group I (sham procedure): a right parietal craniotomy was performed on each animal, and the dura mater was left intact. Group II: experimental brain trauma (EBT) was performed on each animal using a 1 cm inner diameter x 10 cm long glass tube, through which a 20 g weight (0.5 cm diameter) was dropped onto the brain at the craniotomy site, causing a contusional head trauma. Group III: the same EBT model was performed, but 2.5 mg/kg melatonin was injected intraperitoneally four times (total dose 10 mg/kg); these injections were performed 20 min before the operation, during the trauma, 1 h later and 2 h later. The rabbits were sacrificed after the EBT at 24 h after the brain trauma. The activities of the three principal antioxidant enzymes-catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px)-were determined, and the levels of malondialdehyde (MDA), a product of lipid peroxidation, and glutathione (GSH) were measured in brain homogenates. MDA levels were found to be higher in the EBT group than in the EBT+melatonin group or the sham procedure group. The SOD activity was found to be higher in the EBT group than in the sham procedure group. Enzymatic parameters (except for SOD) were significantly higher in melatonin-treated animals than in EBT animals. GSH levels in melatonin-treated animals were decreased compared with EBT animals. In conclusion, the data indicate that melatonin protects against free radical-mediated oxidative changes in brain tissue by boosting antioxidant enzymes, and in particular lowering lipid peroxidation in rabbits with EBT.

Animals↗

PubMed2005

The effects of isoniazid on hippocampal NMDA receptors: protective role of erdosteine.

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.

Animals↗

PubMed2005

Effects of ischemia-reperfusion on NMDA receptor subunits 2a and 2b level in rat hippocampus.

The authors investigated the effects of ischemia and reperfusion on the N-methyl-D-aspartate receptor (NMDAR) subunits 2A and 2B concentration in rat hippocampus. At the protein level, significant increase in the amounts of NMDAR 2A and NMIDAR 2B in the rat hippocampus was observed at 1 h after reperfusion compared with control group. These results suggested that the alteration in hippocampal NMDAR2 subunit concentrations after ischemia-reperfusion might be invovlved in cognitive dysfunction and excitotoxicity.

Animals↗

PubMed2005

EFFECT of nicotine on hippocampal nicotinic acetylcholine alpha7 receptor and NMDA receptor subunits 2A and 2B expression in young and old rats.

Nicotinic acetylcholine (nAChR) and N-methyl-D-aspartate receptors (NMDARs) play critical roles in memory function. This study administered chronic nicotine to determine the alterations of N-methyl-D-aspartate receptor subunit 2A and 2B (NR2A, NR2B) and the alterations of alpha7nAChR receptor. It was determined that the effectivity of nicotine and the data support that nicotine increases hippocampal NR2A and B expression. Additionally, the role of nicotine in the cognitive improvement was not supported by the antioxidative mechanisms or the authors observed no effect of nicotine on lipid peroxidation at the hippocampus.

Age Factors↗

PubMed2004

NMDA receptor subunits 2A and 2B decrease and lipid peroxidation increase in the hippocampus of streptozotocin-diabetic rats: effects of insulin and gliclazide treatments.

Recent studies indicate that diabetes mellitus changes N-methyl-D-aspartate (NMDA) receptor subunit composition and impairs cognitive functions. It also has been known that diabetes mellitus causes lipid peroxidation. This study examined the effects of streptozotocin-diabetes and insulin or gliclazide treatment on the hippocampal NMDA receptor subunit 2A and 2B (NR2A and NR2B) concentrations. In addition, malondial dehyde (MDA) levels were measured as a marker for lipid peroxidation. Eight weeks after the induction of diabetes MDA, levels were increased, and NR2A and NR2B concentrations were reduced. Insulin and gliclazide treatment partially prevented the reduction of NR2A and NR2B expression and prevented the elevation of MDA levels. There was no significant difference between the effects of insulin and gliclazide. The results suggest that the elevation of lipid peroxidation can be the primary biochemical disturbances in diabetes progression, and that changes in NMDA receptor subunit compositions can be involved in cognitive decline in diabetes.

Animals↗

PubMed2004

Effects of dietary long chain PUFAs on hippocampal lipid peroxidation and NMDA receptor subunits A and B concentration in streptozotocin-diabetic rats.

This study examined the effects of streptozotocin (STZ)-diabetes and dietary long chain polyunsaturated fatty acids (LC-PUFAs) on hippocampal N-methyl-D-aspartate (NMDA) receptor subunit expression and lipid peroxidation. MDA level was significantly increased after 8 weeks of STZ-diabetes. LC-PUFAs administration significantly reduced MDA levels in diabetic rats. NR2A and NR2B protein concentrations were significantly decreased by about 30% in diabetic rats. Dietary LC-PUFAs partially restored NR2A and NR2B in diabetic rats whereas the most significant increase was seen in nondiabetic rats. Consequently, dietary LC-PUFAs can partially restore hippocampal NMDA receptors and decrease lipid peroxidation in diabetes. LC-PUFAs are thus a possible prophylactic means for preventing the cognitive deficiencies of diabetes.

Animals↗

PubMed2003

Effect of cigarette smoke on lipid peroxidation, antioxidant enzymes and NMDA receptor subunits 2A and 2B concentration in rat hippocampus.

The effect of cigarette smoke on lipid peroxidation and antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and on the concentration of N-methyl-d-aspartate receptor (NMDAR) subunits 2A and 2B in the hippocampus of Sprague-Dawley rats exposed to cigarette smoke for 2h/day for a period of 4 weeks was determined. It was observed that NMDAR 2A and 2B concentrations in the hippocampus were enhanced in the case of animals exposed to cigarette smoke, whereas lipid peroxidation and antioxidant enzyme activities did not show any change as compared to control animals. The results of our study suggest that cigarette smoke induces NMDAR 2A and 2B expression in the hippocampus, and that this is not due to an increased lipid peroxidation, because cigarette smoke has no effect on lipid peroxidation and antioxidant enzyme activities in the hippocampus.

Animals↗

PubMed2002

Superoxide dismutase and glutathione peroxidase in erythrocytes of patients with iron deficiency anemia: effects of different treatment modalities.

AIM: To test whether the activities of erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) can be affected by oral iron (OI) treatment, parenteral iron (PI) treatment, and parenteral iron treatment with vitamin E supplementation (PIE) in iron deficiency anemia. METHODS: Twenty-eight patients with iron deficiency anemia and 18 healthy controls were included in the study. Anemic patients were systematically allocated into 3 treatment groups. The first group (n=8) received OI, the second group (n=10) PI, and the third group (n=10) PIE. SOD and GSH-Px activities were determined using commercial kits. RESULTS: Before the treatment, SOD activity was significantly lower in anemic patients than in the control group (Kruskal-Wallis test, p<0.05). After the treatment, SOD activity significantly increased in all three patient groups and reached the values found in the control group (Wicoxon signed-rank test, p=0.017 for OI, p=0.047 for PI, and p=0.037 for PIE group). Before the treatment, GSH-Px activities in anemic patients were similar to that of control group (Kruskal-Wallis test, p>0.05). Although there was no significant decrease in GSH-Px activity after OI treatment, both PI and PIE treatments significantly decreased GSH-Px activity (Wilcoxon signed-ranks test, p=0.007 for PI and p=0.005 for PIE). PIE was more effective than PI treatment in maintaining GSH-PX activity. CONCLUSION: Oral iron treatment improved the iron deficiency anemia and recovered antioxidant defense system by increasing SOD activity and maintaining GSH-Px activity at normal level. When parenteral iron treatment is inevitable, vitamin E supplementation together with PI treatment may be effective in partially restoring the antioxidant status in this type of anemia.

Adolescent↗

PubMedDate not supplied

Comparison of the effects of tretinoin, adapalene and collagenase in an experimental model of wound healing.

Adapalene is a new naphthoic acid derivative with strong retinoid agonistic pharmacological properties. We propose that adapalene might contribute to the wound repairing process as is detected with retinoids. In this controlled study, the effects of topical adapalene, tretinoin and collagenase on full-thickness wound healing were compared in an animal model. Thirty-two adult male Wistar-Albino rats were used in the study. Two circular, full-thickness wounds were made for each animal with a standard 8-mm punch biopsy, on both sides of the midline on the back. No treatment was given to Group I rats (n:8) which comprised the control group. Tretinoin cream (0.1%) was applied topically in Group II (n:8), adapalene gel (0.1%) in Group III (n:8), and collagenase ointment in Group IV (n:8) once daily. On day 7, the wounds were photographed to measure the wound surface area. The wounds on the left side of each animal were excised on day 7, for histopathologic and biochemical examination. The treatments were continued for the right side wounds up to 14 days when the same procedure was repeated. In Group II, a significant decrease in hydroxylproline (HP) levels was detected at day 7 (p = 0.018), and an increase at day 14 (p = 0.002) compared to the control group. HP results revealed no difference either in Group III nor in Group IV versus control at day 7 or 14. However, findings of improved healing were more prominent in Groups II and III than the other groups in histopathologic examination. In conclusion, tretinoin and adapalene contributed to the wound healing process resulting in an enhancement of collagen production, angiogenesis and granulation tissue formation.

Adapalene↗

PubMedDate not supplied

The effect of topical corticosteroid on basic fibroblast growth factor in nasal polyp tissue.

BACKGROUND: The etiology of nasal polyposis and pathophysiological mechanisms of polyp formation is still poorly understood. Experimental models have suggested that nasal polyp growth requires extracellular matrix formation and is associated with fibroblast proliferation. Intranasal corticosteroids appear to be useful in reducing nasal polypoid lesions and the likelihood of polyp recurrence after surgery. Basic fibroblast growth factor (bFGF) is a potent angiogenesis factor and is mitogenic for a wide range of cell types. We investigated the alteration of bFGF levels in nasal polyp tissue after administration of topical corticosteroid. METHODS: Nasal polyp tissues were obtained from 36 patients with diffuse nasal polyposis before and after topical nasal steroid treatment. As a topical nasal steroid mometasone furoate was given for 4 weeks in a dosage of 200 microg/day. The bFGF levels were measured by competitive enzyme immunoassay method. RESULTS: The mean levels of tissue bFGF, before and after topical nasal steroid treatment, were 1485 +/- 826 ng/mg protein (range, 416-3434 ng/mg) and 1340 +/- 749 ng/mg protein (range, 330-3288 ng/mg), respectively. The levels of bFGF in nasal polyps were significantly lower than those before treatment after administration of topical nasal steroid (p = 0.011). CONCLUSION: Administration of topical nasal steroid decreases bFGF levels of nasal polyp. It may be suggested that one of the effects in diminishing the size of nasal polyps is by decreasing the bFGF.

Administration, Intranasal↗