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YEGEN, BERRAK

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2005 - 200922010 - 20193
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Author: ŞENER, GÖKSEL × Has files: true ×

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Now showing 1 - 5 of 5
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    PublicationOpen Access
    Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats
    (BIOSCIENTIFICA LTD, 2006-05) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, G.; Kabasakal, L.; Atasoy, B. M.; Erzik, C.; Velioglu-Ogunc, A.; Cetinel, S.; Contuk, G.; Gedik, N.; Yegen, B. C.
    The objective of this study was to examine the potential radioprotective properties of propylthiouracil (PTU)-induced hypothyroidism against oxidative organ damage induced by irradiation. Sprague-Dawley rats were pre-treated with saline or PTU (10 mg/kg i.p.) for 15 days, and were then exposed to whole-body irradiation (800 cGy). A group of rats were decapitated at 6 h after exposure to irradiation, while another group was followed for 72 h after irradiation, during which saline or PTU injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde (MDA; an index of lipid peroxidation) and glutathione (GSH, an antioxidant) levels, myeloperoxidase activity (MPO; an index of tissue neutrophil accumulation) and collagen contents, while oxidant-induced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH), an indicator of tissue damage, and turnout necrosis factor-alpha (TNF alpha) were assayed in serum samples. Irradiation caused a significant decrease in GSH level, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the tissues studied (P < 0.05-0.001). Similarly, serum TNFa and LDH were elevated in the irradiated rats as compared with the control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. Our results suggested that PTU-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.
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    PublicationOpen Access
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    PublicationOpen Access
    Ghrelin against alendronate-induced gastric damage in rats
    (BIOSCIENTIFICA LTD, 2005-12) YEGEN, BERRAK; Iseri, SO; Sener, G; Yuksel, M; Contuk, G; Cetinel, S; Gedik, N; Yegen, BC
    Alendronate sodium, a primary amino bisphosphonate, is widely used in the treatment of various diseases that are associated with bone resorption, such as postmenopausal osteoporosis and Paget's disease of bone. Although the adverse effects of biphosphonates on the gastrointestinal system have been demonstrated in experimental and clinical studies, the exact mechanisms underlying this damage are not clear yet. Ghrelin, a 28 amino acid peptide produced predominantly by the stomach, was shown to exert a potent protective action on the stomach of rats exposed to ethanol or stress. Our objective was to evaluate the possible antioxidant and anti-inflammatory effects of ghrelin against alendronate-induced gastric darnage. Wistar albino rats were administered alendronate (20 mg/kg) by gavage for 4 days, along with either ghrelin (10 ng/kg per day) or saline given i.p. After decapitation, stomach tissues were removed for the determination of malondialdehyde (MIDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and tissue collagen content, while the extent of tissue damage was analyzed microscopically. Formation of reactive oxygen species was determined by chemiluminesence using a Iuminol probe in fresh gastric tissues. Serum tumor necrosis factor (TNF-alpha) and lactate dehydrogenase levels were assessed in trunk blood. Oral administration of alendronate-induced significant gastric damage, accompanied by increased MPO activity, collagen content, MIDA and luminol levels (P < 0(.)01 < P < 0(.)001), while tissue GSH was decreased (P < 0(.)01). On the other hand, ghrelin treatment reversed these alterations (P < 0(.)05-P < 0(.)001) as well as elevating serum TNF-alpha levels significantly (P < 0(.)001). The findings of the present study suggest that alendronate induces oxidative gastric damage by a local irritant effect, and ghrelin amellorates this damage by its possible antioxidant and anti-inflammatory properties.
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    PublicationOpen Access
    Regular swimming exercise performed either before or after the induction of renovascular hypertension alleviates oxidative renal injury in rats
    (2014-05-16) YEGEN, BERRAK; Özdemir Kumral, Zarife Nigar; Şener, Göksel; Yeğen, Berrak Ç.
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    PublicationOpen Access
    Nicorandil preserves blood-brain barrier and improves memory impairment in hypertensive rats
    (MARMARA UNIV, 2019-11-15) YEGEN, BERRAK; Cevikelli Yakut, Zatiye Ayca; Ertas, Busra; Koyuncuoglu, Turkan; Yegen, Berrak C.; Sener, Goksel
    In renovascular hypertension (RVH), oxidative stress and inflammation due to high blood pressure and elevated levels of angiotensin 2 are mainly responsible of cerebrovascular complications and impaired cognitive functions. Since the nicorandil has been shown to exert neuroprotective, anti-inflammatory and antioxidant effects, we investigated the effect of nicorandil against vascular dementia and blood brain barrier damage in a rat model of angiotensin-dependent hypertension. Wistar albino rats, were divided as sham-operated control, renovascular hypertension (RVH) and Nicorandil-treated RVH groups. Silver clip was implanted onto the left renal artery. Using the tail-cuff method, blood pressure of rats was measured before the surgery and at the end of the post-surgical 3rd and 12th weeks. Nicorandil (4mg/kg, orally) or vehicle was administered for 9 weeks. Twelve weeks after RVH surgery, a new object recognition test was performed. Following the determination of blood brain barrier integrity, serum samples were taken for the evaluation of proinflammatory cytokines tumor necrosis alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Levels of sodium-potassium adenosine triphosphatase (Na+/K+-ATPase), as a marker of endothelial damage, were evaluated in the hippocampal tissues. RVH resulted in significant increases in TNF-alpha and IL-1 beta levels and decreases in Na+/K+-ATPase levels, along with impairment in blood brain barrier integrity and memory performance. In the nicorandil treatment group, these indices were reversed back to control levels. The present data demonstrated that nicorandil attenuates RVH-induced memory impairment and blood brain barrier damage in rats with RVH.