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ŞENER, GÖKSEL

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ŞENER

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GÖKSEL

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Now showing 1 - 9 of 9
  • PublicationOpen Access
    The Effects of Calorie Restriction and Exercise on Age-Related Alterations in Corpus Cavernosum
    (FRONTIERS MEDIA SA, 2020-02-18) ŞENER, GÖKSEL; Macit, Caglar; Ustundag, Unsal V.; Dagdeviren, Ozge C.; Mercanoglu, Guldem; Sener, Goksel
    Background Aging is an important risk factor for erectile dysfunction (ED). Both calorie restriction (CR) and physical exercise (PE) have been established as a non-medical method for the improvement of detrimental changes in aging. It is well documented that both CR and PE influence on sympathetic and parasympathetic systems; however, there are few studies on non-adrenergic non-cholinergic pathways. This study aims to investigate the NO-mediated mechanisms of CR and PE on corpus cavernosum in aged rats. Materials and Methods 3 and 15 month-old rats were divided into five experimental groups: young rats fed ad libitum (Y-C), aged rats fed ad libitum (O-S), aged rats with CR (O-CR), aged rats with PE (O-PE), and aged rats with CR and PE (O-CR-PE). CR was applied to animals as a 40% reduction of daily food intake for 6 weeks. PE was moderate swimming at 30 min at 3 days/week. The effects of CR and PE were evaluated by histologic, biologic, and in-vitro tissue bath studies. Results The outcomes in CR and PE groups (characterized by decreased nitrosative damage together with increased antioxidant capacity) were improved in comparison to the O-S. Apoptotic biomarkers were also lower and both endothelial and smooth muscle cell' functions were preserved too. There was no statistical difference between apoptosis, antioxidant capacity, and nitrosative damage parameters. Contractile responses to phenylephrine and relaxation responses to carbachol were: O-CR > O-PE > O-CR-PE. In these groups, NOS protein levels determined by western-blot were: eNOS: O-CR = O-CR + PE > O-PE; iNOS: O-CR = O-PE > O-CR-PE; nNOS: O-PE > O-CR-PE > O-CR. Conclusion In our study, both CR and PE prevented age-related changes in the corpus cavernosum of rats. Reducing nitrosative damage in the neurovascular structure was the main mechanism. CR and exercise restored the endothelial and smooth muscle cells in corpus cavernosum by decreasing apoptosis. The mechanism of enhancing functional response in corpus cavernosum with CR was the improvement of endothelial function via eNOS activation however it involves increases in the NO-cGMP signaling pathway by an endothelium-independent mechanism with PE. This might be a direct stimulation of smooth muscle cells by NO, which released from the cavernous nerve endings via nNOS activation.
  • 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.
  • PublicationOpen Access
    Protective Effects of Origanum onites Essential Oil in the Methotrexate-Induced Rat Model: Role on Apoptosis and Hepatoxicity
    (ACG PUBLICATIONS, 2020-07-27) ÖZBEYLİ, DİLEK; Aykac, Asli; Becer, Eda; Ozbeyli, Dilek; Sener, Goksel; Baser, Kemal Husnu Can
    Methotrexate (MTX) is an effective cytotoxic agent which is used to treat malignancies and inflammatory diseases. Origanum onites (O. onites) is found throughout the Eastern Mediterranean region and has been used in traditional medicine. The essential oils (EOs) of O. onites rich in highly bioactive phytochemicals such as carvacrol (CVR) and has antiviral, antioxidant, anticancer and proapoptotic properties. The aim of this study was to investigate the protective effects of CVR and O. onites-EO treatment in MTX-induced hepatorenal toxic rats' liver and kidney tissues. The bcl-2/bax ratio, glutathione (GSH) level, malondialdehyde (MDA) level, and myeloperoxidase (MPO) activity of liver and kidney tissues were evaluated in the MTX-induced rat model. Results showed that the administration of CVR or O. onites-EO significantly increased bcl-2/bax expression and GSH levels as well as reduced MDA level and MPO activity in the kidney and liver tissues of MTX-induced rat model. In conclusion, our results suggest that O. onites-EO and CVR have protective effect in MTX-induced hepatorenal toxic rats' liver and kidney tissues by decreasing oxidative stress and apoptosis.
  • PublicationOpen Access
    The effect of Cotinus coggygria L. ethanol extract in the treatment of burn wounds
    (2022-01-01) OKUYAN, BETÜL; ŞEN, ALİ; ŞENER, GÖKSEL; ERCAN, FERİHA; Erta B., OKUYAN B., ŞEN A., ERCAN F., Onel H., GÖGER F., Sener G.
    The overall aim of the present research is to evaluate for the first time the curative effect of Cotinus coggygria leaves on burn injury in an experimental burn model along with its anti-inflammatory and antioxidant activity potential. Also, phenolic compounds of C. coggygria were characterised by LC-MS/MS. Wistar albino rats weighing 200-250 g were exposed to 90 degrees C bath for 10 s to induce burn injury, involving 30% of the total body surface area. In the treatment groups, 5% C. coggygria ethanol extract was applied topically as a cream immediately after the burn. Blood and skin tissue samples were taken after decapitation at the 4th and 48th hours following the burn procedure. Interleukin 1-beta (IL-1 beta) and tumour necrosis factor (TNF-alpha) were determined in serum samples, and hydroxyproline, prostoglandin E2 (PGE2), and myeloperoxidase (MPO) activity and 8-hydroxy-2\"-deoxy-guanosine (8-OHdG) levels were determined in skin tissue samples. Increased levels of serum cytokines were decreased with C. coggygria treatment in both periods. MPO activity, prostaglandine (PGE2), and 8-OhdG levels increased, while hydroxyproline levels decreased due to burn damage. On the other hand, these parameters were returned to its normal levels with C. coggygria treatment. In addition, the tissue histology of animals treated with C. coggygria showed a complete epithelialization with increased collagenation. As a result, C. coggygria may be an alternative treatment approach for burns-induced skin damage and wounds.
  • PublicationOpen Access
    The Influence of N-Acetylcysteine Alone and in Combination with Angiotensin Converting Enzyme Inhibitor and Angiotensin Receptor Antagonist on Systemic and Tissue Levels in Rats with Experimentally-Induced Chronic Renal Failure
    (ZOOLOGICAL SOC PAKISTAN, 2020) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sehirli, Ahmet Ozer; Sayiner, Serkan; Velioglu-Ogunc, Ayliz; Serakinci, Nedime; Eksioglu-Demiralp, Emel; Yegen, Berrak; Ercan, Feriha; Sener, Goksel
    The protective effects of ACE inhibitor, Captopril, and angiotensin receptor blocker, Valsartan, were evaluated in the treatment of chronic renal failure (CRF) with and without the presence of N-acetylcysteine (NAC). The renal mass of Wistar albino rats was reduced at a rate of 5/6. Captopril, Valsartan and NAC were applied intra-peritoneal alone or in combination. Blood pressure and heart rate were monitored at weekly intervals over a period of six weeks. Serum creatinine, blood urea nitrogen (BUN), lactate dehydrogenase (LDH) activity, cytokines (TNF-alpha, IL-1 beta, IL-6) concentrations, urinary volume, creatinine, and both serum and urinary electrolyte levels were measured. In addition, the apoptosis rate of white blood cells was analysed from plasma samples. Tissue samples from the brain, heart, aorta and kidneys were used for analysis of the collagen content besides tissue luminol, lucigenin, malondialdehyde (MDA) and glutathione (GSH) levels. A significant difference was determined between the CRF group and the control group with regard to heart rate, blood pressure, serum creatinine, BUN, LDH, cytokines and urinary electrolyte levels. Furthermore, monocyte and neutrophil apoptosis, tissue luminol, lucigenin, malondialdehyde and collagen levels were found to increase. Tissue glutathione levels were found to decrease indicating oxidative damage. These results indicate that oxidative mechanisms induce tissue damage in CRF, and the angiotensin receptor blocker, Valsartan, improved oxidative tissue damage when used in combination with the ACE inhibitor, Captopril or NAC, yielded better results and could be a novel approach for the treatment of CRF when used in combination with anti-oxidants.
  • PublicationOpen Access
    Combination of exercise and caloric restriction ameliorates nearly complete deleterious effects of aging on cardiovascular hemodynamic and antioxidant system parameters
    (MARMARA UNIV, 2020-01-13) ŞENER, GÖKSEL; Macit, Caglar; Ustundag, Unsal, V; Eyupoglu, Ozan E.; Dagdeviren-Cevik, Ozge; Sener, Goksel
    Aging is a progressive and catabolic process by cells of the body are broken down. Study scrutinized the effects of exercise and caloric restriction in cardiovascular hemodynamics and antioxidant system parameters. Rats divided to 5 categories as 1 control group (including 3 months aged animals) and 4 test groups (including 15 months aged animals) named by A-SED (aged-sedentary), A-CR (aged-caloric restricted), A-EX (aged-exercised) and A-CR-EX (aged-(exercised + caloric restricted)) created by adding carbachol (CAR) and phenylephrine (PE) cumulatively and during 6 weeks, 40% caloric restriction and swimming were administered to aged animals. At the beginning and end of study, blood pressure (BP) and ECHO of the animals were measured. After decapitation process, tissue (heart and aorta) samples were collected. In tissue samples, apoptotic and oxidative stress parameters, and in blood samples NO levels were studied. Additionally, tissues were viewed as histologically at light microscopy. GraphPad Prism 5v. program was used for statistics and p<0.05 were considered significantly. Contraction-relaxation responses of aorta improved after CR and EX administrations (p<0.05). In both tissues, oxidative stress parameters (8-OHdG, MDA, SOD, GSH), caspase-3 activity and caspase-3 dansity were recovered meaningfully (p<0.05). Finally, NO levels were significantly recovered with CR and EX administrations in aged animals (p<0.05). To sum up, it is suggested that CR and EX administrations contribute to the recovery of hemodynamic and antioxidant system parameters in aged rats.
  • PublicationOpen Access
    Investigation into the role of the cholinergic system in radiation-induced damage in the rat liver and ileum
    (OXFORD UNIV PRESS, 2014-09-01) ERCAN, FERİHA; Ozyurt, Hazan; Ozden, A. Sevgi; Cevik, Ozge; Ozgen, Zerrin; Cadirci, Selin; Elmas, Merve Acikel; Ercan, Feriha; Sener, Goksel; Goren, M. Z.
    It has been previously shown that acetylcholine (ACh) may affect pro-inflammatory and anti-inflammatory cytokines. The role of the cholinergic system in radiation-induced inflammatory responses and tissue damage remains unclear. Therefore, the present study was designed to determine the radio-protective properties of the cholinergic system in the ileum and the liver of rats. Rats were exposed to 8-Gy single-fraction whole-abdominal irradiation and were then decapitated at either 36 h or 10 d post-irradiation. The rats were treated either with intraperitoneal physiological saline (1 ml/kg), physostigmine (80 mu g/kg) or atropine (50 mu g/kg) twice daily for 36 h or 10 d. Cardiac blood samples and liver and ileal tissues were obtained in which TNF-alpha, IL-1 beta and IL-10 levels were assayed using ELISA. In the liver and ileal homogenates, caspase-3 immunoblots were performed and myeloperoxidase (MPO) activity was analyzed. Plasma levels of IL-1 beta and TNF-alpha increased significantly following radiation (P < 0.01 and P < 0.001, respectively) as compared with non-irradiated controls, and physostigmine treatment prevented the increase in the pro-inflammatory cytokines (P < 0.01 and P < 0.001, respectively). Plasma IL-10 levels were not found to be significantly changed following radiation, whereas physostigmine augmented IL-10 levels during the late phase (P < 0.01). In the liver and ileum homogenates, IL-1 beta and TNF-alpha levels were also elevated following radiation, and this effect was inhibited by physostigmine treatment but not by atropine. Similarly, physostigmine also reversed the changes in MPO activity and in the caspase-3 levels in the liver and ileum. Histological examination revealed related changes. Physostigmine experiments suggested that ACh has a radio-protective effect not involving the muscarinic receptors.
  • PublicationOpen Access
    The effects of riboflavin on ischemia/reperfusion induced renal injury: Role on caspase-3 expression
    (MARMARA UNIV, 2019-05-15) ERTAŞ, BÜŞRA; Ayaz Adakul, Betul; Ertas, Busra; Cevikelli, Zatiye Ayca; Ozbeyli, Dilek; Ercan, Feriha; Kandemir, Cansu; Cevik, Ozge; Sener, Tarik Emre; Sener, Goksel
    Reactive oxygen metabolites play important roles in ischemia/reperfusion (I/R) injury in several organ systems. Riboflavin has been shown to exert antioxidant and/or anti-inflammatory activities in several experimental models. The aim of this study was to investigate the role of riboflavin against I/R injury in the rat kidney. Wistar albino rats 200-300 g weighing were divided into 3 groups. One week after unilateral nephrectomy, the IR procedure was applied to the rats. To induce I/R injury renal pedicle was clamped for 45 minutes and then rats were allowed reperfusion for 6 hours. Riboflavin (25 mg/ kg, orally) or vehicle was administered for one week as pretreatment. After decapitation, kidney tissue samples were taken for the evaluation of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and 8-hydroxydeoxyguanosine (8-OHdG), a specific marker of oxidative DNA damage. Furthermore, myeloperoxidase (MPO) and caspase-3 activities were also examined together with histological analysis. Ischemia/reperfusion induced significant increases in MDA and 8-OHdG levels and MPO and caspase- 3 activities, and decrese in GSH levels. In the riboflavin treatment these indices were found to be reversed back to control levels. The present data demonstrated that riboflavin, through its antioxidant effect, attenuates I/R induced acute renal injury in rats.
  • PublicationOpen Access
    Neuroprotective Effects of Alpha-Lipoic Acid in Experimental Spinal Cord Injury in Rats
    (TAYLOR & FRANCIS LTD, 2010-01) VELİOĞLU ÖĞÜNÇ, AYLİZ; Toklu, Hale Z.; Hakan, Tayfun; Celik, Hasan; Biber, Necat; Erzik, Can; Ogunc, Ayliz V.; Akakin, Dilek; Cikler, Esra; Cetinel, Sule; Ersahin, Mehmet; Sener, Goksel
    Background: Oxidative stress is a mediator of secondary injury to the spinal cord following trauma. Objective: To investigate the putative neuroprotective effect of a-lipoic acid (LA), a powerful antioxidant, in a rat model of spinal cord injury (SCI). Methods: Wistar albino rats were divided as control, vehicle-treated SCI, and LA-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10 was used. Injured animals were given either 50 mg/kg LA or saline at 30 minutes postinjury by intraperitoneal injection. At 7 days postinjury, neurologic examination was performed, and rats were decapitated. Spinal cord samples were taken for histologic examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and DNA fragmentation. Formation of reactive oxygen species in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique. Results: SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in luminol CL and MDA levels, MPO activity, and DNA damage. Furthermore, LA treatment reversed all these biochemical parameters as well as SO-induced histopathologic alterations. Conversely, impairment of the neurologic function caused by SCI remained unchanged. Conclusion: The present study suggests that LA reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, glutathione depletion, and DNA fragmentation.