Person: YÜKSEL, MERAL
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YÜKSEL
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MERAL
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Publication Open Access Effect of Vitamin D Deficiency and Replacement on Endothelial Function in Asymptomatic Subjects(ENDOCRINE SOC, 2009-10-01) VELİOĞLU ÖĞÜNÇ, AYLİZ; Tarcin, Ozlem; Yavuz, Dilek Gogas; Ozben, Beste; Telli, Ahu; Ogunc, Ayliz Velioglu; Yuksel, Meral; Toprak, Ahmet; Yazici, Dilek; Sancak, Seda; Deyneli, Oguzhan; Akalin, SemaContext: Vitamin D receptors are present in many tissues. Hypovitaminosis D is considered to be a risk factor for atherosclerosis. Objective: This study explores the effects of vitamin D replacement on insulin sensitivity, endothelial function, inflammation, oxidative stress, and leptin in vitamin D-deficient subjects. Design, Setting, and Patients: Twenty-three asymptomatic vitamin D-deficient subjects with 25-hydroxyvitamin D [25(OH)D] levels below 25 nmol/liter were compared with a control group that had a mean 25(OH)D level of 75 nmol/liter. The vitamin D-deficient group received 300,000 IU im monthly for 3 months. The following parameters were evaluated before and after treatment: vitamin D metabolites, leptin, endothelial function by brachial artery flow mediated dilatation (FMD), insulin sensitivity index based on oral glucose tolerance test, and lipid peroxidation as measures of thiobarbituric acid reactive substances (TBARS). Results: FMD measurements were significantly lower in 25(OH)D-deficient subjects than controls (P = 0.001) and improved after replacement therapy (P = 0.002). Posttreatment values of TBARS were significantly lower than pretreatment levels (P < 0.001). A positive correlation between FMD and 25(OH)D (r = 0.45; P = 0.001) and a negative correlation between FMD and TBARS (r = -0.28; P < 0.05) were observed. There was a significant increase in leptin levels after therapy, and the leptin levels were positively correlated with 25(OH)D levels (r = 0.45; P < 0.05). Conclusions: This study shows that 25(OH)D deficiency is associated with endothelial dysfunction and increased lipid peroxidation. Replacement of vitamin D has favorable effects on endothelial function. Vitamin D deficiency can be seen as an independent risk factor of atherosclerosis. Hypovitaminosis D-associated endothelial dysfunction may predispose to higher rates of cardiovascular disease in the winter. (J Clin Endocrinol Metab 94: 4023-4030, 2009)Publication Metadata only Protective effects of Ginkgo biloba against acetaminophen-induced toxicity in mice(SPRINGER, 2006) ERCAN, FERİHA; Sener, G; Omurtag, GZ; Sehirli, O; Tozan, A; Yuksel, M; Ercan, F; Gedik, NBackground: The analgesic acetaminophen (AAP) causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. It was reported that these toxic effects of AAP are due to oxidative reactions that take place during its metabolism. Objective: In this study, we aimed to investigate the possible beneficial effect of Ginkgo biloba (EGb), an antioxidant agent, against AAP toxicity in mice. Methods: Balb/c mice were injected i.p. with: (1) vehicle, control (C) group; (2) a single dose of 50 mg/kg Ginkgo biloba extract, EGb group; (3) a single dose of 900 mg/kg i.p. acetaminophen, AAP group, and (4) EGb, in a dose of 50 mg/kg after AAP injection, AAP + EGb group. 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 were measured. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lusigenin probe. Tissues were also examined microscopically. Results: ALT, AST levels, and TNF-alpha were increased significantly (p < 0.001) after AAP treatment, and reduced with EGb. Acetaminophen caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased (p < 0.001) in liver tissues. These changes were reversed by EGb treatment. Furthermore, luminol and lusigenin CL levels in the AAP group increased dramatically compared to control and reduced by EGb treatment (p < 0.01). Conclusion: Our results implicate that AAP causes oxidative damage in hepatic tissues and Ginkgo biloba extract, by its antioxidant effects protects the tissues. Therefore, its therapeutic role as a tissue injury-limiting agent must be further elucidated in drug-induced oxidative damage.Publication Metadata only Effect of phosphodiesterase-5 inhibition on joint and muscle damage in rats with adjuvant arthritis(TUBITAK SCIENTIFIC & TECHNICAL RESEARCH COUNCIL TURKEY, 2018) ERCAN, FERİHA; Bahadir, Faize Elif; Koroglu, Mustafa Kutay; Yuksel, Meral; Ercan, Feriha; Alican, Y. InciBackground/aim: This study was designed to examine the effect of tadalafil, a phosphodiesterase (PDE) 5 inhibitor, on the severity of joint and muscle damage in rats with adjuvant-induced arthritis (AA). Materials and methods: AA was induced by intradermal inoculation into right hind paw of male Sprague Dawley rats (300-450 g) with complete Freund's adjuvant (CFA; 0.1 mL). AA rats were treated with either tadalafil (10 mg/kg; per oral) alone or along with the soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3-a] quinoxalin-1-one (ODQ; 10 mg/kg; intraperitoneally). After decapitation on day 16, trunk blood was collected for total oxidant status (TOS) and total antioxidant capacity (TAC) assays. The left metatarsophalangeal joint and gastrocnemius muscle were excised for microscopic examination. Muscle samples were also evaluated in terms of malondialdehyde (MDA), glutathione, and chemiluminescence (CL) levels. Results: In tadalafil-treated AA rats, metatarsophalangeal joints revealed regular morphology of the cartilage with slight destruction and less inflammatory cell infiltration and vascularization in comparison to the controls (microscopic score: 1.17 +/- 0.31 vs. 4.17 +/- 0.79; P < 0.01). AA rats presented increased gastrocnemius muscle MDA, glutathione, and CL levels compared to the controls (P < 0.01, for MDA; P < 0.05, for glutathione; P < 0.05 for CL). Tadalafil attenuated the increase in CL levels (P < 0.01, for luminol and P < 0.001, for lucigenin). Serum TOS showed significant reductions by tadalafil. Conclusion: The long-acting PDE5 inhibitor tadalafil provides partial protection in a rat model of CFA-induced arthritis possibly via suppression of oxidant generation.Publication Metadata only Alpha-Lipoic Acid Improves Acetic Acid-Induced Gastric Ulcer Healing in Rats(SPRINGER/PLENUM PUBLISHERS, 2009) YEGEN, BERRAK; Karakoyun, Berna; Yuksel, Meral; Ercan, Feriha; Erzik, Can; Yegen, Berrak C.To evaluate the role of ALA treatment on the healing of acetic acid-induced gastric ulcer, rats were given ALA (35 mg/kg/day) or saline for 3 days before the induction of ulcer and the treatment was continued twice daily for 2 days (early) or 10 days (late) until they were decapitated. Gastric ulcer index, microscopic score, elevated DNA fragmentation and chemiluminescence levels of the saline-treated ulcer groups were all reduced by ALA treatment. Likewise, ALA treatment inhibited chemiluminescence levels in both early and late ulcer groups. Marked reduction in glutathione levels of the saline-treated early ulcer group was reversed by ALA treatment, while ALA treatment was effective in depressing gastric myeloperoxidase activity in the late ulcer group. In conclusion, ALA treatment shows protective role in the healing of acetic acid-induced gastric injury in rats via the suppression of neutrophil accumulation, preservation of endogenous glutathione, inhibition of reactive oxidant generation and apoptosis.Publication Metadata only Iron preloading aggravates nutritional steatohepatitis in rats by increasing apoptotic cell death(ELSEVIER, 2007) EREN, FATİH; Imeryuz, Nese; Tahan, Veysel; Sonsuz, Abdullah; Eren, Fatih; Uraz, Suleyman; Yuksel, Meral; Akpulat, Sertac; Ozcelik, Dervis; Haklar, Goncagul; Celike, Cigdem; Avsar, Erol; Tozun, NurdanBackground/Aims: High serum ferritin and liver iron concentrations were found in some patients with NASH, suggesting a role for iron as a co-factor that aggravates liver injury. The aim of this study is to investigate the effects of parenteral iron in a rat model of NASH induced by a methionine choline deficient diet (MCDD). Methods:Wistar rats were divided into 1 - Control, 2 - Iron (Fe), 3 - MCDD, 4 - MCDD&Fe groups. Iron dextran 100 mg/kg was administered intra-muscularly in groups 2 and 4. All rats were fed MCDD, Groups I and 2 were supplied with choline and methionine. Blood and tissue samples were obtained after 4 weeks. Results: The iron injection alone did not affect the liver whereas MCDD led to steatohepatitis. Iron worsened steatosis without any obvious effect on accompanying inflammation. It aggravated tissue injury by increasing apoptosis. Liver fibrosis was observed only in 3 out of 10 rats in the MCDD&Fe group. Conclusions: Observation of liver fibrosis only in the MCDD&Fe group suggests that iron induced increase in apoptosis contributes to the development of fibrosis at an earlier time than expected. (c) 2007 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.Publication Metadata only Antioxidant effect of alpha-lipoic acid against ethanol-induced gastric mucosal erosion in rats(KARGER, 2008) YEGEN, BERRAK; Sehirli, Ozer; Tatlidede, Elif; Yuksel, Meral; Erzik, Can; Cetinel, Sule; Yegen, Berrak C.; Sener, GokselBackground/Aims: This investigation elucidates the role of free radicals in ethanol-induced gastric mucosal erosion and the protective effect of lipoic acid. Methods: After overnight fasting, Wistar albino rats were orally treated with 1 ml of absolute ethanol to induce gastric erosion. Lipoic acid (100 mg/kg) was given orally for 3 days before ethanol administration. Mucosal damage was evaluated 1 h after ethanol administration by macroscopic examination and histological analysis. Additional tissue samples were taken for measurement of malondialdehyde, glutathione (GSH), and myelo-per oxidase activity. Production of reactive oxidants and oxidant-induced DNA fragmentation and Na+,K+-ATPase activity were also assayed in the tissue samples. Results: Generation of reactive oxygen species and lipid peroxidation associated with neutrophil infiltration play an important role in the pathogenesis of gastric mucosal damage induced by ethanol. Furthermore, oxidants depleted tissue GSH stores and impaired membrane structure as Na+,K+-ATPase activity was inhibited. On the other hand, lipoic acid treatment reversed all these biochemical indices as well as the histopathological changes induced by ethanol. Conclusion: These data suggest that lipoic acid administration effectively counteracts the deleterious effect of ethanol-induced gastric mucosal injury and attenuates gastric damage through its antioxidant effects. Copyright (C) 2008 S. Karger AG, Basel.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 Determination of reactive oxygen species in myringotomized tympanic membranes: Effect of vitamin E treatment(WILEY, 2004) HAKLAR, GONCAGÜL; Polat, S; Ozturk, O; Uneri, C; Yuksel, M; Haklar, G; Bozkurt, S; Kullu, SObjectives/Hypothesis: Recent studies have established a strong relationship between the development of myringosclerosis and reactive oxygen species (ROS). The aims of the present study were to directly detect ROS in the tympanic membrane and middle ear mucosa of rats by measuring luminol amplified chemiluminescence, to evaluate the changes in the levels of ROS after treatment with vitamin E, and to examine the possible changes in the tympanic membranes otomicroscopically and histologically. Study Design: Prospective controlled animal study. Methods: Forty healthy Sprague-Dawley rats were divided into five groups of eight animals each. Animals in all groups except group 1 were bilaterally myringotomized. Group 2 received no treatment, group 3 was treated with topical olive oil, group 4 received topical vitamin E, and group 5 received intramuscular vitamin E. After 24 hours of myringotomy, tympanic membranes were examined otomicroscopically; thereafter, tympanic membranes and middle ear mucosa were peeled off. The right ears of the animals were used for biochemical assay, and the left ears were used for histological study. Results: Reactive oxygen species levels were significantly decreased in group 4 with topical application of vitamin E compared with untreated and myringotomized animals in group 2. Reactive oxygen species levels were also decreased in group 5, although the decrease was not statistically significant when compared with groups 2 and 3. Histological studies confirmed sclerotic changes in the untreated myringotomized animals. The tympanic membranes of animals in groups 2 and 3 showed a white, chalk-like pattern of sclerotic changes, whereas animals in groups 4 and 5, with the exception of two animals in group 5, lacked these changes. Conclusion: Although the relationship between the development of myringosclerosis and ROS had been well documented previously, the present study is the first that has directly measured the levels of ROS in the tympanic membrane and middle ear mucosa. These results are relevant because they correlate with histological findings. It has also been demonstrated that topically applied vitamin E is effective in decreasing the ROS levels.Publication Open Access Evaluation of the wound healing potential of Aloe vera-based extract of Nerium oleander(KARE PUBL, 2017) YÜKSEL, MERAL; Akgun, Sevcan Gul; Aydemir, Sezgin; Ozkan, Naziye; Yuksel, Meral; Sardas, SemraOBJECTIVE: Nerium oleander (Apocynaceae) and Aloe vera (Liliaceae) are among the widely used herbal remedies for treating skin diseases and possess numerous activities such as antibacterial, antiviral, antifungal, and antioxidant. The aim of this study was to investigate the possible wound healing effect of Aloev era-based extract of the N. oleander leaf (NAE-8 (R)) based on its antioxidant, anti-inflammatory, and DNA repair capacity along with histological changes and to compare them with the traditional silver sulfadiazine treatment (SSD). METHODS: Twenty-four Wistar albino rats were randomly grouped as follows: i) control, ii) burn alone (burn), iii) burn with topical NAE-8 (R) (burn+ NAE-8 (R)) treatment, and iv) burn with topical 1% silver sulfadiazine (burn+ SSD) treatment. All groups received their related topical application twice a day for 14 consecutive days. Upon completion of the experimental protocol, trunk blood and skin tissues were collected for measuring malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO), tumor necrosis factor alpha (TNF-a), interleukin-1 beta (IL-1 beta), % DNA in the tail (% DNAT) levels along with histological examinations. RESULTS: Thermal injury-induced alterations in MDA, GSH, MPO, TNF-a, IL-1 beta, and % DNAT levels were significantly reversed by NAE-8 (R) treatment. These ameliorative effects were also supported by histological findings. CONCLUSION: Findings of the present study suggest that NAE-8 (R) is a promising remedy for treating skin burn injury.