Person: YÜKSEL, MERAL
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YÜKSEL
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MERAL
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Publication Metadata only The effect of magnesium and vitamin E pre-treatments on irradiation-induced oxidative injury of cardiac and pulmonary tissues in rats: a randomized experimental study(TURKISH SOC CARDIOLOGY, 2012) ATASOY, BESTE MELEK; Atasoy, Beste M.; Ozgen, Zerrin; Bostanci, Korkut; Yuksel, Meral; Ozen, Zeynep; Ibrahimov, Roman; Abacioglu, UfukObjective: The aim of this study was to investigate the effect of pre-treatment with the free radical scavenging molecules, magnesium and vitamin E, on lipid peroxidation to limit radiation-induced heart and lung injury. Methods: Female Sprague-Dawley rats were divided into 4 groups by a simple randomization method as saline-treated control (n=4), saline-treated irradiated (IR; n=6), magnesium sulphate-treated irradiation (IR) (Mg+IR; n=6) and vitamin E-treated IR (vit E+IR; n=6), respectively. The animals were given either saline, Mg (600mg/kg/day) or vit E (100 mg/kg/day) intraperitoneally for five days prior to irradiation. Twelve hours after the fifth injection, animals in irradiation groups were irradiated to 20 Gy using 6 MV photons in linear accelerator. Twenty-four hours later cardiac and lung tissue samples were obtained for determination of myeloperoxidase activity (MPO), malondialdehyde (MDA) levels, and luminol and lucigenin levels measured by chemiluminescence (CL) methods. Results: No significant changes were observed between cardiac and pulmonary MDA and CL results of the experimental groups. However, cardiac and pulmonary MPO activities in the saline-treated IR group were increased as compared to control group (p<0.05 for all), while in the Mg-pretreated and vit E pretreated groups neutrophil infiltration was reduced, reaching to statistical significance only in the Mg-pretreated group (p<0.05). Conclusion: Prophylactic use of magnesium sulfate has limited the infiltration of neutrophils to both the cardiac and pulmonary tissues at the early 24 h of irradiation. However, how limiting neutrophils as the sources of free radicals and inflammatory mediators would alter oxidative stress of heart and lung tissues in the long-term is not clear yet. (Anadolu Kardiyol Derg 2012; 12: 508-14)Publication Metadata only Better lung protection following death due to rapid exsanguination in rats(BAYCINAR MEDICAL PUBL-BAYCINAR TIBBI YAYINCILIK, 2012) LAÇİN, BERNA; Bostanci, Korkut; Lacin, Berna Karakoyun; Yuksel, Meral; Ercan, Feriha; Yuksel, Mustafa; Batirel, Hasan FevziBackground: This study aims to investigate the effects of death due to rapid exsanguination on the viability of lung tissue. Methods: Fourty-six Sprague-Dawley male rats with a weight range of 310-370 g were included in the study. Rats were divided into six groups: (i) ischemic alone (I group; n=8); (ii) passive exsanguination group of whose major abdominal veins were cut following death (PE group; n=8) (iii) group of whose major abdominal veins were cut and sacrified with rapid exsanguination (RE group; n=8); (iv) lung perfusion group with saline (SP group; n=8); (v) lung perfusion group with Perfadex (PP group; n=8) and (vi) control group (C group; n=6). Rats in all experiement groups except rapid exsanguination ones and all in the control group were euthanized with intrahepatic pentobarbital. Lungs were removed following euthanasia in the controls. In all study groups, lungs were ventilated in the cadavers at room temperature for 120 minutes and kept in warm ischemia. Results: Myeloperoxidase (MPO) activity, luminol chemiluminescence (CL) values and non-viable cell rate were higher in the ischemia group. The PE group had increased MPO activity, lucigenin CL values and nonviable cell rate, whereas the RE group had reduced MPO activity and luminol CL values, compared to ischemia group. MPO activity, lucigenin CL levels and non-viable cell rate were lower in the RE group, compared to PE. The PP had lower MPO activity and luminol CL values, compared to SP or ischemia group, whereas non-viable cell rate increased. Conclusion: Death following rapid exsanguination results in better preservation of lung viability and minimal oxidative injury. This may be explained by rapid loss of platelets and inflammatory cells in the tissue and shift of extravascular fluid to intravascular compartment.Publication Metadata only THERAPEUTIC POTENTIAL OF MYRTUS COMMUNIS SUBSP COMMUNIS EXTRACT AGAINST ACETIC ACID-INDUCED COLONIC INFLAMMATION IN RATS(WILEY, 2017) ŞEN, ALİ; Sen, Ali; Yuksel, Meral; Bulut, Gizem; Bitis, Leyla; Ercan, Feriha; Ozyilmaz-Yay, Nagehan; Akbulut, Ozben; Cobanoglu, Hamit; Ozkan, Sevil; Sener, GokselThe aim of this study was to evaluate the effect of ethanol extract from leaves of Myrtus communis subsp. communis (MC) on acetic acid (AA)-induced ulcerative colitis in rats. On the fourth day of colitis induction, all rats were decapitated. Colitis was assessed by macroscopic and microscopic scores and by measuring malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, luminol, lucigenin, nitric oxid and peroxynitrite chemiluminescence (CL). Colitis caused significant increases in the colonic MDA levels, MPO activity, CL values, macroscopic and microscopic damage scores along with significant decrease in tissue GSH level. However, treatment with MC extract reversed all these biochemical indices, as well as histopathological alterations induced by AA with the protective effects being similar to that of sulphasalazine treatment. The study showed that MC extract could alleviate colitis in rats and can be considered an alternative therapeutic approach for management of inflammatory bowel diseases (IBD).Publication Metadata only alpha-lipoic acid protects against renal ischaemia-reperfusion injury in rats(BLACKWELL PUBLISHING, 2008) YÜKSEL, MERAL; Sehirli, Oezer; Sener, Emre; Cetinel, Ule; Yueksel, Meral; Gedik, Nursal; Sener, Goeksel1. Oxygen free radicals are important components involved in the pathophysiological processes observed during ischaemia-reperfusion (I/R). The present study was designed to assess the possible protective effect of et-lipoic acid (ALA) on renal I/R injury. 2. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min renal pedicle occlusion followed by 24 h reperfusion. Saline or ALA (100 mg/kg, i.p.) was administered 15 min prior to ischaemia and immediately before the reperfusion period. At the end of 24 h, rats were decapitated and trunk blood was collected. Creatinine, blood urea nitrogen (BUN) and lactate dehydrogenase (LDH) activity were measured in serum samples, whereas tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6, 8-hydroxydeoxyguanosine (8-OHdG) and total anti-oxidant capacity (AOC) were assayed in plasma samples. 3. Kidney samples were taken for the determination of tissue malondialdehyde (MDA) and glutathione (GSH) levels, as well as Na/K-ATPase and myeloperoxidase (MPO) activity. The formation of reactive oxygen species in renal tissue samples was monitored using a chemiluminescence (CL) technique with luminol and lucigenin probes. Oxidant-induced tissue fibrosis was determined by tissue collagen content and the extent of tissue injury was analysed microscopically. 4. Ischaemia-reperfusion caused a significant increases in blood creatinine, BUN, LDH, IL-1 beta, IL-6, TNF-alpha and 8-OHdG, whereas AOC was decreased. In kidney samples from the I/R group, MDA, MPO, collagen and CL levels were found to be increased significantly; however, glutathione levels and Na/KATPase activity were decreased. Conversely, ALA treatment reversed all these biochemical indices, as well as histopathological alterations induced by I/R. 5. In conclusion, these data suggest that ALA reverses I/R-induced oxidant responses and improves microscopic damage and renal function. Thus, it seems likely that ALA protects kidney tissues by inhibiting neutrophil infiltration, balancing the oxidant-anti-oxidant status and regulating the generation of inflammatory mediators.Publication Metadata only The role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat(ELSEVIER IRELAND LTD, 2013) VELİOĞLU ÖĞÜNÇ, AYLİZ; Kolgazi, Meltem; Uslu, Unal; Yuksel, Meral; Velioglu-Ogunc, Ayliz; Ercan, Feriha; Alican, InciThe cholinergic anti-inflammatory pathway'' provides neurological modulation of cytokine synthesis to limit the magnitude of the immune response. This study aimed to evaluate the impact of the cholinergic anti-inflammatory pathway on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Colitis was induced by intrarectal administration of 5% acetic acid (1 ml) to Sprague-Dawley rats (200-250 g; n = 7-8 per group). Control group received an equal volume of saline intrarectally. The rats were treated with either nicotine (1 mg/kg/day) or huperzine A (0.1 mg/kg/day) intraperitoneally for 3 days. After decapitation, the distal colon was scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Formation of reactive oxygen species was monitored by using chemiluminescence (CL). Nuclear factor (NF)-kappa B expression was evaluated in colonic samples via immunohistochemical analysis. Trunk blood was collected for the assessment of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-10, resistin and visfatin levels. Both nicotine and huperzine A reduced the extent of colonic lesions, increased colonic MDA level, high MPO activity and NF-kappa B expression in the colitis group. Elevation of serum IL-1 beta level due to colitis was also attenuated by both treatments. Additionally, huperzine A was effective to reverse colitis-induced high lucigenin-enhanced CL values and serum TNF-alpha levels. Colitis group revealed decreased serum visfatin levels compared to control group which was completely reversed by nicotine. In conclusion, modulation of the cholinergic system either by nicotine or ACh esterase inhibition improved acetic acid-induced colonic inflammation as confirmed by macroscopic and microscopic examination and biochemical assays. (C) 2013 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only The effect of sildenafil, a phosphodiesterase-5 inhibitor, on acetic acid-induced colonic inflammation in the rat(WILEY, 2009) ERCAN, FERİHA; Iseri, Sevgin Ozlem; Ersoy, Yasemin; Ercan, Feriha; Yuksel, Meral; Atukeren, Pinar; Gumustas, Koray; Alican, InciSildenafil, a selective and potent inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase (PDE)5, has a relaxant effect on the smooth muscle cells of the arterioles supplying the human corpus cavernosum acting via nitric oxide (NO)-dependent mechanism. This study aimed to investigate the possible protective effect of sildenafil citrate on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Colitis was induced by intrarectal administration of 1 mL of 5% acetic acid to Sprague-Dawley rats (200-250 g; n = 7-8/group). Control rats received an equal volume of saline intrarectally. In treatment groups, the rats were treated with either sildenafil citrate (5 mg/kg/day; subcutaneously) or saline for 3 days. After decapitation, distal colon was weighed and scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and oxidant production. Trunk blood was collected for the assessment of serum tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta levels. In the colitis group, the colonic tissue was characterized by lesions, increased lipid peroxidation with a concomitant reduction in GSH content, increased MPO activity and oxidant production. Serum TNF-alpha and IL-1 beta levels were higher in the colitis group compared to control values. Sildenafil reversed these inflammatory parameters nearly back to control values. Sildenafil citrate administration to rats with acetic acid-induced colitis seems to be beneficial via prevention of lipid peroxidation, oxidant generation, cytokine production and neutrophil accumulation.Publication Metadata only Alpha Lipoic Acid Alleviates Oxidative Stress and Preserves Blood Brain Permeability in Rats with Subarachnoid Hemorrhage(SPRINGER/PLENUM PUBLISHERS, 2010) YEGEN, BERRAK; Ersahin, Mehmet; Toklu, Hale Z.; Cetinel, Sule; Yuksel, Meral; Erzik, Can; Berkman, M. Zafer; Yegen, Berrak C.; Sener, GoekselThe neuroprotective effect of alpha lipoic acid (ALA; 100 mg/kg, po), a dithiol antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) was assessed in Wistar albino rats. Neurological examination scores recorded at the 48th h of SAH induction were increased in SAH groups, which were accompanied with significant increases in the formation of reactive oxygen species, DNA fragmentation ratios, malondialdehyde levels and myeloperoxidase activity, while significant decreases in the brain glutathione content and Na+, K+-ATPase activity were observed. On the other hand, ALA treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations. Increased brain edema, impaired blood-brain-barrier permeability and neurological scores were also improved by ALA treatment. The results demonstrate that ALA exerts neuroprotective effects via the enhancement of endogenous antioxidant enzyme activity, the inhibition of neutrophil accumulation and free radical generation, suggesting a therapeutic potential in reducing secondary injury after SAH in patients.Publication Metadata only Simvastatin attenuates cisplatin-induced kidney and liver damage in rats(ELSEVIER IRELAND LTD, 2007) ERCAN, FERİHA; Iseri, Sevgin; Ercan, Feriha; Gedik, Nursal; Yuksel, Meral; Alican, InciStatins have anti-inflammatory effects that are not directly related to their cholesterol-lowering activity. This study aimed to investigate the effect of simvastatin on the extent of tissue damage in cisplatin-induced nephrotoxicity and hepatotoxicity. The rats received a single intravenous injection of 2.5 mg kg(-1) cisplatin. Other groups received either simvastatin (1 mg kg(-1)) or the vehicle (ethanol: saline) intraperitoneally for 10 days beginning 5 days prior to cisplatin injection. All animals were decapitated 5 days after cisplatin administration. Trunk blood was collected and analyzed for blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), albumin, and total bilirubin levels. The urine samples were used for the calculation of creatinine clearance levels. The kidney and liver samples were stored for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content or were processed for histopathological examinations. Formation of reactive oxygen species in tissue samples was monitored by using chemiluminescence method. Simvastation reduced the extent of both kidney and liver damage and preserved both kidney and liver functions (p < 0.01-0.001). Increase in liver MDA level with a concomitant reduction in GSH in the cisplatin group was attenuated by simvastatin treatment (p < 0.05-0.01). Increase in tissue collagen content and chemiluminescence levels in the kidney and liver samples of the cisplatin group was also reversed by simvastatin (p < 0.001). In conclusion, simvastatin is beneficial in cisplatin-induced kidney and liver dysfunction and organ damage in rats via prevention of lipid peroxidation and tissue fibrosis, preservation of antioxidant glutathione, and suppression of neutrophil infiltration. (c) 2006 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only Silymarin, the antioxidant component of Silybum marianum, protects against burn-induced oxidative skin injury(ELSEVIER SCI LTD, 2007) ERCAN, FERİHA; Toklu, Hale Z.; Tunah-Akbay, Tuba; Erkani, Gozde; Yuksel, Meral; Ercan, Feriha; Sener, GokselBackground: Despite recent advances, severe burn is one of the most common problems faced in the emergency room. Major thermal injury induces the activation of an inflammatory cascade resulting in local tissue damage, to contribute to the development of subsequent damage of multiple organs distant from the original burn wound. Objective: Silymarin, the major component of milk thistle has been shown to have antioxidant properties. In the present study, we investigated the putative antioxidant effect of local or systemic silymarin treatment on burn-induced oxidative tissue injury. Methods: Wistar albino rats were exposed to 90 degrees C bath for 10 s to induce burn. Silymarin either locally (30 mg/kg) applied on 4 cm(2) area or locally + systemically (50 mg/kg, p.o.) was administered after the burn and repeated twice daily. Rats were decapitated 48 h after injury and blood was collected for tumor necrosis factor-a (TNF-alpha) and lactate dehydrogenase (LDH) activity. In skin tissue samples malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and luminol-lucigenin chemiluminescense (CL) were measured in addition to the histological evaluation. Results: Burn caused a significant increase in TNF-a and LDH levels. MDA levels were increased and GSH levels were decreased in the skin at 48 h after-burn. Both local and systemic silymarin treatments significantly reversed these parameters. The raised MPO activity and luminol-lucigenin CL were also significantly decreased. Conclusion: Results indicate that both systemic and local administration of silymarin was effective against burn-induced oxidative damage and morphological alterations in rat skin. Therefore, silymarin merits consideration as a therapeutic agent in the treatment of burns. (C) 2006 Elsevier Ltd and ISBI. All rights reserved.Publication Metadata only Rosiglitazone attenuates liver inflammation in a rat model of nonalcoholic steatohepatitis(SPRINGER, 2007) ÇELİKEL, ÇİĞDEM; Tahan, Veysel; Eren, Fatih; Avsar, Erol; Yavuz, Dilek; Yuksel, Meral; Emekli, Ebru; Imeryuz, Nese; Celikel, Cigdem; Uzun, Hafize; Haklar, Goncagul; Tozun, NurdanRosiglitazone is an insulin-sensitizing agent. We aimed to assess the effects of rosiglitazone on a methionine- and choline-deficient diet (MCDD) model of nonalcoholic steatohepatitis (NASH) in rats. Wistar rats were fed either MCDD or a control diet in the 4-week induction study; they were given saline or 4 mg/kg/day rosiglitazone. After the induction study period, the rats were divided into four groups and fed MCDD or given a control diet for an additional 8 weeks and received saline or rosiglitazone. Serum and tissue samples were obtained. Rosiglitazone improved inflammation in NASH and improved ALT, alkaline phosphatase, and interleukin-6 levels in the induction study and interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha levels in the treatment study. Our preliminary study is the first to show the anti-inflammatory effects of rosiglitazone in NASH. Rosiglitazone's effect on cytokines may be a key mechanism of its anti-inflammatory effect in NASH.