Person: YEGEN, BERRAK
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YEGEN
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BERRAK
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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 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 Halofuginone improves caustic-induced oxidative injury of esophagus in rats(SPRINGER JAPAN KK, 2018) YEGEN, BERRAK; Cerit, Kivilcim Karadeniz; Karakoyun, Berna; Bahadir, Elif; Yuksel, Meral; Bulbul, Nurdan; Ercan, Feriha; Dagli, E. Tolga; Yegen, Berrak C.The aim of this study is to evaluate the anti-inflammatory and anti-fibrotic effects of halofuginone in caustic esophageal burn injury in rats. Corrosive esophageal injury (CEI) was produced in male Wistar albino rats by instilling NaOH solution (1 ml, 37.5%) into the distal esophagus. Rats were decapitated on the 3rd day (early group) or 28th day (late group), and treated daily with either saline or halofuginone (100 A mu g/kg/day; i.p.), continued on alternate days after the third day. Histopathological evaluation and measurement of nitric oxide (NO), peroxynitrite (ONOO-) and oxygen-derived radicals by chemiluminescence (CL) were made in the distal 2 cm of the esophagus. Non-irrigated proximal esophageal samples were assessed for the levels of nuclear factor (NF)-kappa B, caspase-3, glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) activity. GSH, MDA, NF-kappa B and caspase-3 levels, and MPO activity in the proximal esophagus were not different among groups. Increased number of TUNEL (+) cells in the irrigated esophagus of the early and late caustic injury groups was reduced by halofuginone treatment. High microscopic damage scores in both early and late CEI groups were decreased with halofuginone treatment. NO, ONOO- and CL levels, which were elevated in the saline-treated early CEI group, were reduced by halofuginone treatment, but reduced NO and ONOO- levels in the late period of saline-treated group were increased by halofuginone. In addition to its anti-fibrotic effects, current findings demonstrate that halofuginone exerts antioxidant and anti-apoptotic actions and supports therapeutic potential for halofuginone in CEI-induced oxidative stress.Publication Metadata only The effects of Nigella sativa against oxidative injury in a rat model of subarachnoid hemorrhage(SPRINGER WIEN, 2011) YEGEN, BERRAK; Ersahin, Mehmet; Toklu, Hale Z.; Akakin, Dilek; Yuksel, Meral; Yegen, Berrak C.; Sener, GokselThe aim of the study was to investigate the putative neuroprotective effect of Nigella sativa oil (NSO) treatment against subarachnoid hemorrhage (SAH) in rats. To induce SAH, rats were injected with 0.3 ml blood into their cisterna magna. Male Wistar albino rats were divided as control, vehicle-treated SAH, and NSO-treated (0.2 ml/kg, intraperitoneally) SAH groups. Forty-eight hours after SAH induction, neurological examination scores were recorded and the rats were decapitated. Brain tissue samples were taken for blood brain barrier permeability, brain water content, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+-K+-ATPase activities. On the second day of SAH induction, neurological examination scores were increased in SAH groups, while SAH caused significant decreases in brain GSH content and Na+-K+-ATPase activity, which were accompanied with significant increases in MDA levels and MPO activity. The histological observation showed vasospasm of the basillary artery. On the other hand, NSO treatment markedly improved the neurological scores while all oxidant responses were prevented, implicating that NSO treatment may be of therapeutic use in preventing oxidative stress due to SAH.Publication Open Access A 10-day mild treadmill exercise performed before an epileptic seizure alleviates oxidative injury in the skeletal muscle and brain tissues of the rats(2022-01-01) KAYA, ÖZLEM TUĞÇE; YEGEN, BERRAK; YÜKSEL, MERAL; YILDIRIM, ALPER; Arabaci -Tamer S., KAYA Ö. T., YÜKSEL M., YILDIRIM A., YEGEN B.© 2022 Marmara University Press, All Rights Reserved.Objective: Epileptic seizures may cause skeletal muscle injury and memory dysfunctions. The present study was aimed to investigate the possible protective effects of exercising prior to seizure on seizure-induced oxidative injury in the skeletal muscle and brain. Materials and Methods: Sprague-Dawley male rats were assigned as non-exercise (n=16) and exercise groups (n=16). Following a 3-day exercise training, exercise protocol (30 min) was performed on a treadmill for 10 days, while control rats had no exercise. On the 11th day, the epileptic seizure was induced by a single intraperitoneal injection of pentylenetetrazol (PTZ) (45 mg/kg), while the control groups were injected with saline. Passive-avoidance test was initially performed before PTZ/saline injection and repeated 72 h later for the assessment of memory function. Brain and gastrocnemius muscles were taken for histological assessments and to determine the levels of malondialdehyde (MDA) and glutathione (GSH), myeloperoxidase (MPO) activity and luminal – and lucigenin – enhanced chemiluminescence levels. Results: Exercise training alone increased the formation of reactive oxygen species and elevated the antioxidant GSH capacity of the muscle tissue in the control rats, but these effects were not observed in the muscles of the exercised rats induced with a PTZ-seizure. On the other hand, short-term exercise alone had no effect on the basal oxidative parameters of the brain tissues. Prior exercise did not alter the average seizure scores or memory performances when compared to non-exercised groups, but suppressed the PTZ-induced elevations in MDA and chemiluminescence levels as well as MPO activity in the brain. Conclusion: A 10-day mild treadmill exercise reduced the oxidative brain damage due to a single seizure-induced excitotoxicity and exerted a preconditioning effect on the skeletal muscles exposed to tonic-clonic contractions.