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Agmatine attenuates intestinal ischemia and reperfusion injury by reducing oxidative stress and inflammatory reaction in rats

Turan, İnci | Özaçmak-Sayan, Hale | Özaçmak, Veysel Haktan | Barut, Figen | Araslı, Mehmet

Article | 2017 | Life Sciences189 , pp.23 - 28

Aims Oxidative stress and inflammatory response are major factors causing several tissue injuries in intestinal ischemia and reperfusion (I/R). Agmatine has been reported to attenuate I/R injury of various organs. The present study aims to analyze the possible protective effects of agmatine on intestinal I/R injury in rats. Main methods Four groups were designed: sham control, agmatine-treated control, I/R control, and agmatine-treated I/R groups. IR injury of small intestine was induced by the occlusion of the superior mesenteric artery for half an hour to be followed by a 3-hour-long reperfusion. Agmatine (10 mg/kg) was administer . . .ed intraperitoneally before reperfusion period. After 180 min of reperfusion period, the contractile responses to both carbachol and potassium chloride (KCl) were subsequently examined in an isolated-organ bath. Malondialdehyde (MDA), reduced glutathione (GSH), and the activity of myeloperoxidase (MPO) were measured in intestinal tissue. Plasma cytokine levels were determined. The expression of the intestinal inducible nitric oxide synthase (iNOS) was also assessed by immunohistochemistry. Key findings The treatment with agmatine appeared to be significantly effective in reducing the MDA content and MPO activity besides restoring the content of GSH. The treatment also attenuated the histological injury. The increases in the I/R induced expressions of iNOS, IFN-?, and IL-1? were brought back to the sham control levels by the treatment as well. Significance Our findings indicate that the agmatine pretreatment may ameliorate reperfusion induced injury in small intestine mainly due to reducing inflammatory response and oxidative stress. © 2017 Elsevier Inc Daha fazlası Daha az

Rosiglitazone treatment reduces hippocampal neuronal damage possibly through alleviating oxidative stress in chronic cerebral hypoperfusion

Özaçmak-Sayan, Hale | Özaçmak, Veysel Haktan | Barut, Figen | Jakubowska-Doğru, Ewa

Article | 2012 | Neurochemistry International61 ( 3 ) , pp.287 - 290

Oxygen free radicals and lipid peroxidation may play significant roles in the progress of injury induced by chronic cerebral hypoperfusion of the central nervous system. Rosiglitazone, a well known activator of PPAR?, has neuroprotective properties in various animal models of acute central nervous system damage. In the present study, we evaluate the possible impact of rosiglitazone on chronic cerebral hypoperfused-rats in regard to the levels of oxidative stress, reduced glutathione, and hippocampal neuronal damage. Chronic cerebral hypoperfusion was generated by permanent ligation of both common carotid arteries of Wistar rats for . . .one month. Animals in treatment group were given rosiglitazone orally at doses of 1.5, 3, or 6 mg/kg per day of the 1 month duration. The treatment significantly lowered the levels of both malondialdehyde and neuronal damage, while elevated the reduced glutathione level markedly. These findings suggest that the beneficial effect of rosiglitazone on hypoperfusion-induced hippocampal neuronal damage might be the result of inhibition of oxidative insult. © 2012 Elsevier Ltd. All rights reserved Daha fazlası Daha az

Chronic treatment with resveratrol, a natural polyphenol found in grapes, alleviates oxidative stress and apoptotic cell death in ovariectomized female rats subjected to chronic cerebral hypoperfusion

Özaçmak, Veysel Haktan | Özaçmak-Sayan, Hale | Barut, Figen

Article | 2016 | Nutritional Neuroscience19 ( 4 ) , pp.176 - 186

Objectives: Resveratrol appears to have neuroprotective potential in various animal models of brain disorders including cerebral ischemia and neurodegenerative diseases. Chronic cerebral hypoperfusion is a well-known pathological condition contributing to the neurodegenerative diseases such as vascular dementia. Purpose of the present study is to evaluate the possible therapeutic potential of resveratrol in a model of vascular dementia of ovariectomized female rats. Assessment of the potential was based on the determination of brain oxidative status, caspase-3 level, glial fibrillary acidic protein (GFAP), and neuronal damage on hip . . .pocampus and cerebral cortex. Methods: For creating the model of chronic cerebral hypoperfusion, ovariectomized female Wistar rats were subjected to the modified two vessel occlusion method, with the right common carotid artery being occluded first and the left one a week later. Results: At the 15th day following the ligation, neuronal damage was accompanied by the increased immunoreactivities of both GFAP and caspase-3, and significant neurodegeneration was evident in the hippocampus and cortex, all of which were significantly alleviated with resveratrol treatment (10 mg/kg). Biochemical analysis revealed that the resveratrol treatment decreased lipid peroxidation and restored reduced glutathione level as well. Discussion: The collected data of the present study suggest that the administration of resveratrol may provide a remarkable therapeutic benefit for vascular dementia, which is most likely related to the prevention of both apoptotic cell death and oxidative stress. We believe that therapeutic efficacy of resveratrol deserves to be tested for potential clinical application in postmenopausal elderly women suffering from vascular dementia. © 2015 W. S. Maney & Son Ltd 2015 Daha fazlası Daha az

Protective effect of melatonin on contractile activity and oxidative injury induced by ischemia and reperfusion of rat ileum

Özaçmak, Veysel Haktan | Sayan, Hale | Arslan, S. Oktay | Altaner, Şemsi | Aktaş, R.Gülhan

Article | 2005 | Life Sciences76 ( 14 ) , pp.1575 - 1588

Free radicals derived from molecular oxygen have been reported to be responsible for changes in motility and mucosal damage observed in intestinal ischemia-reperfusion injury. Melatonin has been considered as an antioxidant that prevents injuries resulted from I/R in various tissues. The present study was designed to determine the effect of melatonin on the contractile responses of acetylcholine (Ach) and KCl, on malondialdehyde (MDA), a product of lipid peroxidation, and reduced glutathione (GSH) levels and to assess histopathological changes in the smooth muscle of terminal ileum subjected to ischemia-reperfusion. The intestinal i . . .schemia-reperfusion was induced by occlusion of superior mesenteric artery of rat for 30 min, followed by a period of reperfusion for 3 h. Melatonin at doses of 10 or 50 mg/kg was administered via the tail vein in 5 min prior to reperfusion. Following reperfusion, segments of terminal ileum were rapidly taken and transferred into isolated organ bath and responses to Ach and KCl were recorded. Samples of terminal ileum were also taken for measuring the MDA and GSH levels. EC50 values of these contracting substances were seriously reduced in the ischemia-reperfusion group compared to that of the sham-operated control group. The decreased contraction response to Ach and KCl was significantly ameliorated by a dosage of 50 mg/kg of melatonin, while not by a dosage of 10 mg/kg. Similar pattern of the effect was observed in the tissue levels of MDA and GSH as well as in histological improvement. Melatonin appeared to be restoring the amounts of tissue MDA and GSH back to about control levels. These results suggest that the high dose of melatonin not only physiologically but also biochemically and morphologically could be useful to normalize contractility injured by oxidative stress in intestinal ischemia-reperfusion. © 2004 Elsevier Inc. All rights reserved Daha fazlası Daha az

Attenuation of contractile dysfunction by atorvastatin after intestinal ischemia reperfusion injury in rats

Özaçmak, Veysel Haktan | Sayan, Hale | Akyıldız-İğdem, Ayşenur | Çetin, Alpay | Özaçmak, İhsan Diler

Article | 2007 | European Journal of Pharmacology562 ( 01.Feb ) , pp.138 - 147

Growing number of studies implicate that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, have beneficial effects on ischemia/reperfusion injury that are unrelated to their cholesterol-lowering action. In the present study, we aimed to evaluate possible effects of atorvastatin on oxidative stress, neutrophil accumulation, and contractile response of terminal ileum segments in rats subjected to intestinal ischemia/reperfusion. Intestinal ischemia/reperfusion model was generated by clamping the superior mesenteric artery for 30 min followed by reperfusion for 3 h. Oral administration of atorvastatin at a dose of . . . 10 mg/kg/day lasted 3 days just before induction of intestinal ischemia. At the end of reperfusion period, terminal ileum samples were removed to determine the concentrations of malondialdehyde, reduced glutathione, and myeloperoxidase. Samples were collected also to assess histopathological alterations and contractile response to agonists. Ischemia/reperfusion significantly decreased contractile responses, and this decrease was attenuated by atorvastatin. Pretreatment with atorvastatin caused remarkable decrease in both oxidative stress and neutrophil accumulation. Atorvastatin appeared to be restoring amount of reduced glutathione back to about control level. Furthermore, the pretreatment lowered mucosal damage at histopathological level. Our results suggested that pretreatment with atorvastatin attenuated intestinal muscle dysfunction associated with ischemia/reperfusion. This remarkable effect of atorvastatin is accomplished at least by decreasing oxidative stress and neutrophil accumulation as well as preventing the depletion of reduced glutathione. © 2007 Elsevier B.V. All rights reserved Daha fazlası Daha az

L-Arginine and melatonin interaction in rat intestinal ischemia--reperfusion.

Arslan, S. Arslan | Gelir, Ethem | Sayan, Hale | Özaçmak, Veysel Haktan

Article | 2005 | Fundamental & clinical pharmacology19 ( 5 ) , pp.533 - 535

We investigated the combinative effects of L-arginine and melatonin on the contractile responses of terminal ileum after the intestinal ischemia-reperfusion (I/R), in vivo. Male rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (180 min). We have observed a dramatic decrease in spontaneous basal activity and Ach-induced contractile response. Our data clearly showed that the contractility decrease was ameliorated by L-arginine but not by L-NAME. Melatonin has reversed the inhibition of contractility caused by I/R injury in part. We did not observe an augmentation in the contractility of ileum when we use mel . . .atonin and L-arginine in combination, in fact, melatonin decreased the protective effect of L-arginine in intestinal I/R injury Daha fazlası Daha az

Colonic tuberculosis mimicking tumor perforation: A case report and review of the literature

Cömert-Beğendik, Füsun | Cömert, Mustafa | Külah, Canan | Taşçılar, Öge | Numanoğlu, Gamze | Aydemir, Selim

Article | 2006 | DIGESTIVE DISEASES AND SCIENCES51 ( 6 ) , pp.1039 - 1042

3rd European Meeting on Molecular Diagnostics -- 37910 -- Scheveningen, NETHERLANDS WOS: 000239295700002 PubMed: 16865564

Beneficial effects of melatonin on reperfusion injury in rat sciatic nerve

Sayan, Hale | Özaçmak, Veysel Haktan | Özen, Oğuz Aslan | Coşkun, Ömer | Arslan, S. Oktay | Sezen, S. Cem | Aktaş, R. Gülhan

Article | 2004 | Journal of Pineal Research37 ( 3 ) , pp.143 - 148

Studies have shown that ischemia-reperfusion (I/R) produces free radicals leading to lipid peroxidation and to damage of the nervous tissue. Melatonin, a main secretory product of the pineal gland, has free radical scavenging and antioxidant properties and has been shown to diminish I/R injury in many tissues. There are a limited number of studies related to the effects of melatonin on I/R injury in the peripheral nervous system. Therefore, in the present study, the protective effect of melatonin was investigated in rats subjected to 2 hr of sciatic nerve ischemia followed by 3 hr of reperfusion. Following reperfusion, nerve tissue . . .samples were collected for quantitative assesment of malondialdehyde (MDA). an oxidative stress marker, and superoxide dismutase (SOD), a principal antioxidant enzyme. Samples were further evaluated at electron microscopic level to examine the neuropathological changes. I/R elevated the concentration of MDA significantly while there was a reduction at SOD levels. Melatonin treatment reversed the I/R-induced increase and decrease in MDA and SOD levels, respectively. Furthermore, melatonin salvaged the nerve fibers from ischemic degeneration. Histopathologic findings in the samples of melatonin-treated animals indicated less edema and less damage to the myelin sheaths and axons than those observed in the control samples. Our results suggest that administration of melatonin protects the sciatic nerve from I/R injury, which may be attributed to its antioxidant property Daha fazlası Daha az

Analysis of glomerular filtration rate, serum cystatin C levels, and renal resistive index values in cirrhosis patients

Üstündağ, Yücel | Samsar, Ufuk | Açıkgöz, Şereften | Çabuk, Mehmet | Kıran, Sibel | Külah, Eyüp | Aydemir, Selim

Article | 2007 | Clinical Chemistry and Laboratory Medicine45 ( 7 ) , pp.890 - 894

Background: The aim of this study was to evaluate the relation of glomerular filtration rate (GFR) to serum cystatin C levels, renal resistive index (RRI), serum creatinine and creatinine clearance in patients with different stages of cirrhosis. Methods: The study sample was 25 cirrhotic patients (10 females and 15 males; mean age 57.3±2.04 years), 10 in the compensated stage without ascites and 15 in the decompensated stage with new-onset ascites. None had azotemia nor were on diuretic treatment. The control group comprised 25 healthy adults (11 female and 14 men; mean age 56.56±1.91 years). Serum cystatin C, RRI, serum creatinine . . .and creatinine clearance were measured. GFR was determined by technetium99m- diethylene triamine pentaacetic acid renal scintigraphy. Results: Cirrhosis cases had lower mean scintigraphic GFR than controls (64.5±4.03 vs. 87.96±4.16 mL/min, p<0.05). Serum cystatin C and RRI were significantly higher in the cirrhotic group compared to controls (1.16±0.09 mg/L and 0.68±0.01 vs. 0.86±0.03 mg/L and 0.64±0.01, respectively; p<0.05). Subgroup comparative analysis showed that only two parameters, scintigraphic GFR and serum cystatin C, were significantly different between compensated and decompensated cirrhotics (75.62±4.9 mL/min and 0.89±0.07 mg/L vs. 57.23±5.14 mL/min and 1.34±0.13mg/L, respectively; p<0.05). Scintigraphic GFR showed significant correlation with cystatin C, but not with serum creatinine or creatinine clearance (r=-0.877, p<0.05) in decompensated patients. No correlation was observed between scintigraphic GFR and RRI or between serum cystatin C and RRI in all subjects. A receiver operator characteristics curve showed that cystatin C at a cutoff value of 1.01 mg/L can significantly differentiate patients with GFR <70 mL/min with 80% sensitivity and 80% specificity. Conclusions: Serum cystatin C, but not serum creatinine or RRI measurement, correlates with GFR in each stage of liver failure and has a significant diagnostic advantage in detecting lower GFR in such cases. © 2007 by Walter de Gruyter Daha fazlası Daha az

PMMA-multigraft copolymers derived from linseed oil, soybean oil, and linoleic acid: Protein adsorption and bacterial adherence

Çakmaklı, Birten | Hazer, Baki | Açıkgöz, Şerefden | Can, Murat | Cömert, Füsun B.

Article | 2007 | Journal of Applied Polymer Science105 ( 6 ) , pp.3448 - 3457

Synthesis of Poly(methyl methacrylate), PMMA-multigraft copolymers derived from linseed oil, soybean oil, and linoleic acid PMMA-g-polymeric oil/oily acid-g-poly(3-hydroxy alkanoate) (PHA), and their protein adsorption and bacterial adherence have been described. Polymeric oil/oily acid peroxides [polymeric soybean oil peroxide (PSB), polymeric linseed oil peroxide (PLO), and polymeric linoleic acid peroxide (PLina)] initiated the copolymerization of MMA and unsaturated PHA-soya to yield PMMA-PLO-PHA, PMMA-PSB-PHA, and PMMA-PLina-PHA multigraft copolymers. PMMA-PLina-PHA multigraft copolymers were completely soluble while PMMA-PSB-P . . .HA and PMMA-PLO-PHA multigraft copolymers were partially crosslinked. Crosslinked parts of the PLO- and PSB-multigraft copolymers were isolated by the sol gel analysis and characterized by swelling measurements in CHCl3. Soluble part of the PLO- and PSB-multigraft copolymers and completely soluble PLina-multigraft copolymers were obtained and characterized by spectroscopic, thermal, gel permeation chromatography (GPC), and scanning electron microscopy (SEM) techniques. In the mechanical properties of the PHA-PLina-PMMA, the elongation at break is reduced up to ~ 9%, more or less preserving the high stress values at its break point (48%) when compared to PLina-g-PMMA. The solvent casting film surfaces were studied by means of adsorption of blood proteins and bacterial adhesion. Insertion of the PHA into the multigraft copolymers caused the dramatic increase in bacterial adhesion on the polymer surfaces. PHA insertion into the graft copolymers also increased the protein adsorption. © 2007 Wiley Periodicals. Inc Daha fazlası Daha az

The effects of 17 beta estradiol, 17 alpha estradiol and progesterone on oxidative stress biomarkers in ovariectomized female rat brain subjected to global cerebral ischemia

Özaçmak, Veysel Haktan | Sayan, Hale

Article | 2009 | Physiological Research58 ( 6 ) , pp.909 - 912

Neuroprotective effects of estrogens and progesterone have been widely studied in various experimental models. The present study was designed to compare possible neuroprotective effects of 17alpha-estradiol, 17beta-estradiol, and progesterone on oxidative stress in rats subjected to global cerebral ischemia. Global cerebral ischemia was induced in ovariectomized female rats by four vessel occlusion for 10 min. Following 72 h of reperfusion, levels of malondialdehyde (MDA, oxidative stress marker), and reduced glutathione (GSH, major endogenous antioxidant) were assessed in hippocampus, striatum and cortex of rats treated with either . . . 17alpha-estradiol, 17beta-estradiol, progesterone or estradiol + progesterone beforehand. Steroid administration ameliorated ischemia-induced decrease in GSH and increase in MDA levels. Our data offers additional evidence that estrogens and progesterone or combination of two exert a remarkable neuroprotective effect reducing oxidative stress. © 2009 Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic Daha fazlası Daha az

AT1 receptor blocker candesartan-induced attenuation of brain injury of rats subjected to chronic cerebral hypoperfusion

Özaçmak, Veysel Haktan | Sayan, Hale | Çetin, Alpay | Akyıldız-İğdem, Ayşenur

Article | 2007 | Neurochemical Research32 ( 8 ) , pp.1314 - 1321

One of common pathophysiological states associated with central nervous system is chronic cerebral hypoperfusion (CH) that frequently occurs in conditions such as vascular dementia and Alzheimer's disease. Long term blockage of angiotensin II type 1 (AT 1 ) receptor provides protection from ischemia induced injury of brain as well as reduction of cerebrovascular inflammation. Examining effect of the blockage on reduced glutathione (GSH), ascorbic acid (AA), and lipid peroxidation were of purpose in the present study. Modeling CH, rats were subjected to permanent occlusion of common carotid arteries bilaterally. AT 1 receptor antagon . . .ist, candesartan, was given daily for 14 days after surgery. CH caused a significant increase in lipid peroxidation and decrease in GSH content of cerebral hippocampal tissue with no change in AA level. Candesartan (0.5 mg/kg, oral) not only reduced lipid peroxidation but also restored GSH significantly besides elevating AA and improving histopathological alterations. In conclusion, long term AT 1 receptor blockage may be considered as novel therapeutic approach for protection from damage associated with CH. Underlying mechanism(s) may in part be related to suppressing oxidative stress and preserving brain antioxidant capacity. © 2007 Springer Science+Business Media, LLC Daha fazlası Daha az

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