Person: ÇETİNEL, ŞULE
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ÇETİNEL
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ŞULE
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Publication Metadata only Antioxidant Agent Quercetin Prevents Impairment of Bladder Tissue Contractility and Apoptosis in a Rat Model of Ischemia/Reperfusion Injury(WILEY, 2017) TİNAY, İLKER; Tinay, Ilker; Sener, Tarik E.; Cevik, Ozge; Cadirci, Selin; Toklu, Hale; Cetinel, Sule; Sener, Goeksel; Tarcan, TufanObjectivesTo examine the possible protective effect of quercetin (QT), which is well known for its antioxidant and protective effects in circumstances of oxidative stress, on urinary bladder tissue in a rat model of ischemia/reperfusion (I/R) injury, which is a known factor for the development of lower urinary tract dysfunction partly mediated by the generation of free radicals causing oxidative damage. MethodsThirty male Sprague-Dawley rats were subjected to I/R injury through clamping the abdominal aorta for 30 min and then allowing reperfusion for the next 60 min. Quercetin (20 mg/kg; subcutaneously) or vehicle were given before ischemia and just before reperfusion. Findings of the isometric contraction studies in the organ bath and of the histological examinations along with oxidative stress markers were evaluated in bladder tissues. ResultsIncreased malondialdehyde (MDA) levels and myeloperoxidase (MPO) activities and decreased glutathione (GSH) levels and superoxide dismutase (SOD) activities in the I/R group were reduced by QT treatment. In the I/R group, pro-apoptotic marker caspase-3 was increased and anti-apoptotic bcl-2 protein was decreased, while QT treatment significantly reversed these parameters. In the I/R group contractile responses of the bladder strips to carbachol were significantly lower than those of the control group, which were reversed by QT treatment. ConclusionQuercetin treatment protects bladder tissue contractility against acute I/R injury by decreasing oxidative stress and apoptosis induced by I/R.Publication Metadata only Mesna (2-mercaptoethane sulfonate) prevents ischemia/reperfusion induced renal oxidative damage in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2004) ŞENER, GÖKSEL; Kabasakal, L; Sehirli, AO; Cetinel, S; Cikler, E; Gedik, N; Sener, GReoxygenation of the ischemic tissue promotes the generation of various reactive oxygen metabolites (ROM) which are known to have deleterious effects on various cellular functions. This study was designed to determine the possible protective effect of mesna (2-Mercaptoethane Sulfonate) on renal ischemia/reperfusion (I/R) injury. Wistar albino rats were unilaterally nephrectomized, and 15 days later they were subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Mesna (MESNA, 150 mg/kg, i.p.; an effective dose against I/R injury) or vehicle was administered twice, 15 min prior to ischemia and immediately before the reperfusion period. At the end of the reperfusion period, rats were killed by decapitation. Kidney samples were taken for histological examination or determination of the free radicals, renal malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Renal tissue collagen content, as a fibrosis marker was also determined. Creatinine and urea concentrations in blood were measured for the evaluation of renal function. The results demonstrated that renal I/R caused nephrotoxicity, as evidenced by increases in blood urea and creatinine levels, which was reversed by MESNA treatment. Increased free radical levels, as assessed by nitroblue-tetrazolium test were reduced with MESNA. Moreover, the decrease in GSH and increases in MDA levels, and MPO activity induced by I/R indicated that renal injury involves free radical formation. Treatment of rats with MESNA restored the reduced GSH levels while it decreased MDA levels as well as MPO activity. Increased collagen contents of the kidney tissues by I/R were reversed back to the control levels by MESNA treatment. Since MESNA administration reversed these oxidant responses, improved renal function and microscopic damage, it seems likely that MESNA protects kidney tissue against I/R induced oxidative damage. (C) 2004 Elsevier Inc. All rights reserved.Publication Metadata only Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice(ELSEVIER SCIENCE BV, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Sener, GokselThe protective effect of beta-glucan against oxidative injury caused by acetaminophen was studied in mice liver. BALB-c mice (25-30 g) were pretreated with beta-D-glucan (50 mg/kg, p.o.) for 10 days and on the 11th day they received an overdose of acetaminophen (900 mg/kg, i.p.). Four hours after the acetaminophen injection, mice were decapitated and their blood was taken to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels. Tissue samples of the liver were taken for histological examination or for the determination of levels of malondialdehyde, an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase activity, an index of tissue neutrophil infiltration. The formation of reactive oxygen species in hepatic tissue samples was monitored by using the chemilummescence technique with luminol and lucigenin probes. Acetaminophen caused a significant decrease in the GSH level of the tissue, which was accompanied with significant increases in the hepatic luminol and lucigenin chemiluminescence values, malondialdehyde level, MPO activity and collagen content. Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. On the other hand, P-D-glucan treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by acetaminophen. In conclusion, these results suggest that beta-D-glucan exerts cytoprotective effects against oxidative injury through its antioxidant properties and may be of therapeutic use in preventing acetaminophen toxicity. (c) 2006 Elsevier B.V. All rights reserved.Publication Metadata only Protective effects of resveratrol against acetaminophen-induced toxicity in mice(WILEY, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, Goksel; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Gedik, NursalThis investigation elucidates the role of free radicals in acetaminophen (AA)-induced toxicity and the possible protection by resveratrol (RVT). BALB-c mice were injected with a single dose of 900 mg/kg AA to induce toxicity, while RVT administred in a dose of 30 mg/kg i.p. following AA. Mice were sacrificed 4 h after AA injection to determine serum ALT, AST and tumor necrosis factor-alpha (TNF-alpha) levels in blood, and glutathione (GSH), malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity and collagen contents in liver tissues. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probe. ALT, AST levels and TNF-alpha were increased significantly after AA treatment, and reduced with RVT. AA caused a significant decrease in GSH levels while MDA levels and MPO activity were increased in liver tissues. On the other hand when RVT administered following AA, depletion of GSH and accumulation of MDA and neutrophil infiltration were reversed back to control. Furthermore increased luminol and lucigenin CL levels in the AA group reduced by RVT treatment. Our results implicate that AA causes oxidative damage in hepatic tissues and RVT, by its potent antioxidant effects protects the liver tissue. These data suggest that RVT may be of therapeutic use in preventing hepatic oxidative injury due to AA toxicity. (c) 2006 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only The antifibrotic drug halofuginone reduces ischemia/reperfusion-induced oxidative renal damage in rats(ELSEVIER SCI LTD, 2013) YEGEN, BERRAK; Cerit, Kivilcim Karadeniz; Karakoyun, Berna; Yuksel, Meral; Ozkan, Naziye; Cetinel, Sule; Dagli, E. Tolga; Yegen, Berrak C.; Tugtepe, HalilAim: The objective of the present study was to evaluate the protective effects of halofuginone against renal ischemia/reperfusion (I/R) injury. Materials and methods: Male Wistar albino rats were unilaterally nephrectomized and the left renal pedicles were occluded for 45 min to induce ischemia and then reperfused for 6 h (early) or for 72 h (late). The rats were treated intraperitoneally with either halofuginone (100 mu g/kg/day) or saline 30 min prior to ischemia and the dose was repeated in the late reperfusion groups. In the sham groups, rats underwent unilateral nephrectomy and were treated at similar time points. The animals were decapitated at either 6 h or 72 h of reperfusion and trunk blood and kidney samples were obtained. Results: I/R injury increased renal malondialdehyde levels, myeloperoxidase activity and reactive oxygen radical levels, and decreased the renal glutathione content. Halofuginone treatment was found to reduce oxidative I/R injury and improve renal function in the rat kidney, as evidenced by reduced generation of reactive oxygen species, depressed lipid peroxidation and myeloperoxidase activity, and increased glutathione levels. Conclusions: The present findings demonstrate the anti-inflammatory and antioxidant effects of halofuginone in renal I/R injury, supporting its potential use where renal I/R injury is inevitable. (C) 2012 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.Publication Metadata only The effects of spironolactone in preventing bile duct ligation-induced hepatitis in a rat model(Iranian Journal of Pharmaceutical Research, 2021) VELİOĞLU ÖĞÜNÇ, AYLİZ; Özer Şehirli A., Kökeş A., Velioğlu-öğünç A., Tetik Ş., Özkan N., Çetinel Ş., Sayıner S., Dülger G.Cholestasis is associated with the accumulation of bile acids and bilirubin in the hepatocytes and leads to liver injury. Pregnane X Receptor (PXR) coordinates protective hepatic responses to toxic stimuli, and this receptor was reported to stimulate bile secretion by increasing MRP2 expression. Since PXR activators were reported to be anti-inflammatory in the liver, PXR was proposed as a drug target for the treatment of chronic inflammatory liver diseases. We investigated the potential protective effect of spironolactone (SPL), an enzyme inducer, in hepatotoxicity induced by bile duct ligation in rats. Wistar Albino (250-300 g) rats were divided into the control group and the bile duct ligated (BDL) group. BDL group was divided into three subgroups; following BDL, for 3 days, the first group received propylene glycol (vehicle of SPL) (blinded), the second subgroup received spironolactone (SPL) (200 mg/kg oral), and the third subgroup received SPL for 3 days, starting 3 days after the bile duct ligation, in order to investigate if it has a healing effect after hepatitis had developed. The control group was sham-operated and received saline. At the end of the experiment, blood and tissue samples were collected. Serum TNF-α, NF-ĸB, bilirubin, IL-6 levels, ALT, AST, ALP activities and tissue MPO activity and oxidant damage increased after the bile duct ligation was significantly decreased following SPL administration. PXR and MRP2 activity showed an increase in the hepatocytes as a result of the treatment. In conclusion, it was observed that SPL administration significantly decreases liver inflammation and damage related to BDL. © 2021, Iranian Journal of Pharmaceutical Research. All rights reserved.Publication Metadata only Erdosteine prevents colonic inflammation through its antioxidant and free radical scavenging activities(SPRINGER, 2007) AKSOY, HALİL; Sener, Goeksel; Aksoy, Halil; Sehirli, Oezer; Yueksel, Meral; Aral, Cenk; Gedik, Nursal; Cetinel, Sule; Yegen, Berrak C.After intracolonic administration of trinitrobenzene sulphonic acid (TNBS), Sprague-Dawley rats were treated orally either with saline or erdosteine (100 mg/kg per day), a sulfhydryl-containing antioxidant, for 3 days. On the 4th day, rats were decapitated and distal colon was removed for the macroscopic and microscopic damage scoring, for the measurement of malondialdehyde (MDA), glutathione (GSH) and collagen levels, myeloperoxidase (MPO) activity, luminol and lucigenin chemiluminescences (CL) and DNA fragmentation. Lactate dehydrogenase (LDH) activity, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, and antioxidant capacity were assayed in blood samples. Colitis caused significant increases in the colonic CL values, macroscopic and microscopic damage scores, MDA and collagen levels, MPO activity and DNA fragmentation, along with a significant decrease in tissue GSH level. Similarly, serum cytokines and LDH were elevated in the saline-treated colitis group as compared with the control group. On the other hand, erdosteine treatment reversed all these biochemical indices, and histopathologic alterations induced by TNBS, suggesting that erdosteine protects the colonic tissue via its radical scavenging and antioxidant activities.Publication Open Access Could Ambroxol reduce cytokines in hepatic ischemia-reperfusion injury in rats(2022-01-01) ÇETİNEL, ŞULE; Gulfekin C., Sehirli A. O., Cetinel S., Sayiner S.OBJECTIVES: The aim of the study is to examine the effect of Ambroxol on TNF-α and IL-1β released after liver ischemia-reperfusion injury. BACKGROUND: Many drugs are being tried to reduce ischemia-reperfusion injury, which is life threating problem after many liver surgeries. In this study, it was investigated whether Ambroxol reduces the release of pro-infl ammatory cytokines released after liver ischemia-reperfusion injury. METHODS: Twenty-four Wistar albino rats were divided into 3 groups as Control (CTR; n=8), hepatic ischemia reperfusion (H-IR; n=8) and hepatic ischemia reperfusion+Ambroxol (H-IR+AMB; n=8). In H-IR+AMB group, Ambroxol (30 mg/kg) was administered orally 30 minutes before ischemia period. In H-IR and H-IR+AMB groups underwent 45 minutes of hepatic ischemia followed by a 60-minute reperfusion period. After reperfusion period, tissue and blood samples were collected from euthanised animals. ALT, AST, ALP, LDH, TNF-α, IL-1β concentrations and liver tissues were evaluated. RESULTS: Serum ALT, ALP, AST, LDH, TNF-α and IL-1β values were lower in the H-IR+AMB group compared to the H-IR group. In the histopathological examination, hepatocyte degeneration and congestion in the H-IR group were higher than in the H-IR+AMB group.Publication Metadata only Intradetrusor botulinum neurotoxin A (BoNT-A) injections decrease bladder fibrosis secondary to partial urethral obstruction in the male rat model(WILEY, 2012) TİNAY, İLKER; Tinay, Ilker; Tanidir, Yiloren; Cikler, Esra; Cetinel, Sule; Tarcan, TufanAims We evaluated effects of BoNT-A injections on bladder function and histomorphology in a male-rat-overactive-bladder model, created by partial urethral obstruction.Publication Metadata only Nesfatin-1 treatment preserves antioxidant status and attenuates renal fibrosis in rats with unilateral ureteral obstruction(2022-06-01) ÇETİNEL, ŞULE; YEGEN, BERRAK; KAYA, ÖZLEM TUĞÇE; ÖZBEYLİ, DİLEK; Tezcan N., Özdemir-Kumral Z. N., Yenal N. Ö., Çilingir-Kaya Ö. T., Virlan A. T., Özbeyli D., Çetinel Ş., Yeğen B., Koç M.Background Nesfatin-1 (NES-1), an anorexigenic peptide, was reported to have anti-inflammatory and anti-apoptotic actions in several inflammation models. Methods To elucidate potential renoprotective effects of NES-1, unilateral ureteral obstruction (UUO) was induced in male Sprague Dawley rats by ligating left ureters. The rats were injected intraperitoneally with either saline (SL) or NES-1 (10 mu g/kg/day) for 7 or 14 days (n = 8 in each group). On the 7th or 14th day, obstructed kidneys were removed for the isolation of leucocytes for flow-cytometric analysis and the assessments of biochemical and histopathological changes. Results Opposite to glutathione levels, renal myeloperoxidase activity in the SL-treated UUO group was significantly increased compared with the sham-operated group, while NES-1 treatment abolished the elevation. The percentages of CD8+/CD4+ T-lymphocytes infiltrating the obstructed kidneys were increased in the SL-treated groups but treatment with NES-1 did not prevent lymphocyte infiltration. Elevated tumour necrosis factor-alpha (TNF-alpha) levels in SL-treated UUO group were decreased with NES-1. Although total degeneration scores were similarly increased in all UUO groups, tubular dilatation scores were significantly increased in UUO groups and lowered by NES-1 only in the 7-day treated group. Elevated interstitial fibrosis scores in the SL-treated groups were decreased in both 7- and 14-day NES-1 treated groups, while alpha-smooth muscle actin (alpha-SMA) and apoptosis scores were depressed in both NES-1 treated groups. Conclusion The present data demonstrate that UUO-induced renal fibrosis is ameliorated by NES-1, which appears to involve the inhibition of neutrophil infiltration and thereby amelioration of oxidative stress and inflammation. These data suggest that NES-1 may have a regulatory role in protecting the kidneys against obstruction-induced renal injury.