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YEGEN, BERRAK

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YEGEN

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BERRAK

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Now showing 1 - 10 of 36
  • 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.
  • PublicationOpen Access
    Ghrelin Treatment Improves Lipid Metabolism and Hepatic Degeneration in Ovariectomized Rats
    (GAZI UNIV, FAC MED, 2020-01-01) YEGEN, BERRAK; Gurler, Esra Bihter; Ozbeyli, Dilek; Kaya, Ozlem Tugce Cilingir; Ercan, Feriha; Yegen, Berrak C.
    Objective: Metabolic disorders occurring in post-menopausal period increase the risk for development of fatty liver disease in women. Aim of the study was to evaluate possible effects of ghrelin on metabolic biomarkers and hepatic morphology in ovariectomized (OVT) rats. Methods:Under ketamine-chlorpromazine anesthesia (100 mg/kg, 0.75 mg/kg), Sprague-Dawley rats (n=12) underwent bilateral OVT, while control group had sham-surgery (n=6). Four weeks after surgery, half of OVT rats were treated intraperitonally with ghrelin (1 mg/kg/hafta) for 4 weeks, while others were not treated. Rats were euthanized by cardiac puncture at the end of 8th weeks, and serum levels of glucose, insulin, aspartate aminotransferase (AST), high-density lipoprotein (HDL), low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), triglycerides, estradiol and progesterone were measured by an automated analyzer. Results: Increased body weights in OVT rats (p<0.001) recorded at the end of 2 months was not changed with ghrelin. Serum estradiol and progesterone levels were reduced (p<0.05) verifying altered gonadal hormone status, but insulin and glucose levels were not changed. Reduced HDL and increased LDL levels (p<0.0.5) were evident in non-treated OVX rats, while ghrelin treatment depressed LDL levels (p<0.0.5), but did not change HDL levels. However, ghrelin in OVT rats depressed triglycerides, VLDL and AST levels significantly (p<0.05). Moderate sinusoidal congestion, activated Kupffer cells and hepatocytes with ballooning degeneration was observed in non-treated OVT rats, while significant improvements were present in livers of ghrelin-treated rats. Conclusion: In conclusion, mild dyslipidemia and hepatic degeneration in early post-menopausal period appear to be attenuated by ghrelin treatment, and require further investigation.
  • PublicationOpen Access
    Peripheral administration of neuropeptide W inhibits gastric emptying in rats: the role of small diameter afferent fibers and cholecystokinin receptors
    (2023-02-10) YEGEN, BERRAK; Tamer S. A., Yeğen B.
    Neuropeptide W (NPW), a novel hypothalamic peptide, contributes to the central regulation of food intake and energy balance, and suppresses feeding behavior when administered centrally. The aim of our study was to investigate the role of peripherally administered NPW in the modulation of gastric emptying, and to evaluate the participation of afferent fibers, cholecystokinin (CCK) receptors and gastric smooth muscle contractility in the regulatory effects of NPW on gastric motility. In Sprague-Dawley male rats equipped with gastric fistula, gastric emptying rate of the saline and peptone solutions was measured following subcutaneous administration of NPW (0.1 or 5 μg/kg) preceded by subcutaneous injections of saline, CCK-1 or CCK-2 receptor antagonists. Another group of rats with cannulas were injected subcutaneously with capsaicin for afferent denervation before commencing emptying trials. The effect of NPW on carbachol-induced gastric contractility and the role of CCK receptors in gastric smooth muscle contractility were also assessed in gastric strips. Peripheral injection of NPW delayed gastric emptying rate of both caloric and non-caloric liquid test meals, while administration of CCK-1 or CCK-2 receptor antagonists or denervation of small diameter afferents reversed NPW–induced delay in gastric emptying. Moreover, NPW inhibited antrum contractility in the organ bath. Our results revealed that peripherally administered NPW delayed liquid emptying from the stomach via the involvement of small diameter afferent neurons and CCK receptors, and thereby this regulatory role may contribute to its central regulatory role in controlling food intake and energy balance.
  • PublicationOpen Access
    The effects of resveratrol treatment on caveolin-3 expression and Na+/K+ ATPase activity in rats with isoproterenol-induced myocardial injury
    (KARE PUBL, 2020) YEGEN, BERRAK; Sehirli, Ahmet Ozer; Aykac, Asli; Tetik, Sermin; Yiginer, Omer; Cetinel, Sule; Ozkan, Naziye; Akkiprik, Mustafa; Kaya, Zehra; Yegen, Berrak Caglayan; Tezcan, Mehmet; Sener, Goeksel
    OBJECTIVE: The present study aims to investigate the therapeutic effects of resveratrol (RES) on isoproterenol (ISO) induced myocardial injury rat model. METHODS: Catecholamine-induced heart damage was induced by ISO treatment for 30 days. The rats were divided into four groups as follows: the control group received saline, the ISO group received 5.0 mg/kg ISO, the RES group received 10 mg/kg RES, and the ISO-RES group received 10 mg/kg RES and 5 mg/kg ISO treatments for 30 days. Following echocardiographic measurements and body weight recorded, the rats were decapitated. Plasma and cardiac tissue samples obtained by decapitation were analyzed using biochemical, histopathological, molecular and immunohistochemical methods. RESULTS: In the ISO group, Na+/K+ ATPase activity and ATP content, GSH, and caveolin-3 levels were low. LDH, CK and lysosomal enzyme activities, MDA level, and MPO activity were found to be high. It was determined that GSH and MDA levels and MPO, Na+/K+ ATPase activity, ATP content caveolin-3 levels changes that arose from ISO treatment were suppressed by RES treatment. CONCLUSION: RES treatment has ameliorated all the functional and biochemical parameters. The results obtained in this study suggest that RES is a promising supplement against catecholamine exposure as it improves antioxidant defense mechanisms in the heart. In the light of above-mentioned data, RES can be assumed as a promising agent in ameliorating the oxidative injury of the myocardium.
  • PublicationOpen Access
    The potency of obestatin in improving kidney functions and apoptosis in rats with cisplatin-induced acute kidney injury
    (2022-01-01) ÖZDEMİR KUMRAL, ZARİFE NİGAR; BULUT, ALİSİNA; ÖZKAN YENAL, NAZİYE; YEGEN, BERRAK; KOÇ, MEHMET; ÖZDEMİR KUMRAL Z. N. , BULUT A., Üzülmez B., Vezirhüyük M., Kök Z., ÖZKAN YENAL N., YEGEN B., KOÇ M.
    © 2022 Marmara University Press.Cisplatin (CP), which is the most commonly used anticancer agent to treat several solid tumors, may cause acute kidney injury (AKI) as the major limiting factor for its clinical use. Obestatin (OB) is a ghrelin gene-derived peptide produced in several tissues and has shown anti-oxidant, anti-apoptotic, and anti-inflammatory effects in many experimental models. This study investigated the effect of OB treatment on nephrotoxicity induced by CP. Rats were divided into 4 groups as two control (1 ml/kg, saline, intraperitoneal (ip), single dose) and two CP-induced (7 mg/kg, ip, single dose) AKI groups (8 rats in each group). Immediately after the CP injection and the following two days, injections of OB (10 µg/kg, ip) were performed. Rats were decapitated at the end of 72 hours. Blood and kidney tissue samples were taken for biochemical and histopathological measurements. The results of the present study revealed that serum creatinine and BUN levels were significantly increased in the CP-induced AKI group when compared to the control group. Treatment with OB improved kidney functions and ameliorated renal oxidative injury and maintained oxidative balance in the CP-induced AKI model, which was revealed by elevated malondialdehyde and depleted glutathione levels. TUNEL scores also demonstrated that CP increased the apoptotic response, while OB treatment abolished it. CP-induced medullary and cortical injuries were also partially reversed by OB treatment. Thus, our findings show that OB alleviates CP-induced nephrotoxicity in rats through the abolishment of oxidative stress and apoptosis.
  • PublicationOpen Access
    Neuropeptide w alleviates hepatorenal oxidative damage in sepsis-induced rats
    (2020-05-01) ATICI, ALİ EMRE; PEKER EYÜBOĞLU, İREM; ERCAN, FERİHA; AKKİPRİK, MUSTAFA; YEGEN, BERRAK; ATICI A. E., ARABACI TAMER S., levent h. n., PEKER EYÜBOĞLU İ., ERCAN F., AKKİPRİK M., YEGEN B.
    Background: Despite modern surgical, medical and intensive care treatments, sepsis is still one of the most frequent causes of morbidity and mortality due to multiple life-threatening organ dysfunctions. We aimed to investigate the possible protective effect of neuropeptide W (NPW), a novel peptide effective in regulating neuroendocrine functions, against sepsisinduced hepatorenal damage. Methods: In male Sprague-Dawley rats (200–250 g), sepsis was induced by cecal ligation and puncture under ketamine anesthesia (n=48). Immediately after surgery, saline or TNF-alpha inhibitor (etanercept; 1 mg/kg) plus antibiotic (ceftriaxon; 100 mg/kg) (ET+C) or NPW (0.1, 0.3, 1 or 3 mg/kg) was given subcutaneously, and repeated at 12th and 24th hours, while sham-operated control group (n=8) received three saline injections within twenty-four hours. Rats were decapitated at the 25th hour of surgery and C-reactive protein (CRP), corticosterone and IL-6 levels were measured in serum samples. Kidney and liver samples were obtained for the measurement of myeloperoxidase activity (MPO), malondialdehyde and glutathione levels and nuclear factor kappa-B (NF-kB) mRNA expression levels. Histopathological evaluations were performed in hematoxylin-eosin-stained samples. ANOVA and Student's t-tests were used for data analysis. Results: Elevated serum levels of IL-6, corticosterone and CRP (p<0.05-0.01) in saline-treated sepsis group, as compared to controls, were depressed in the ET+C- (p<0.05) or NPW- (p<0.05-0.001) treated groups. Hepatic malondialdehyde and MPO levels, which were increased in salinetreated sepsis group (p<0.05 and p<0.001), were decreased by ET+C- (p<0.01) or NPW (p<0.05-0.001) treatments. Similarly, increased renal malondialdehyde level was depressed by NPW (p<0.05), but not by ET+C; while none of the treatments had an inhibitory effect on renal MPO. In contrast to replenished renal glutathione levels by all treatments, hepatic glutathione content was not changed by any of the treatments. Hepatic and renal NF-kB mRNA expressions were similar in all groups. Severe hepatocyte degeneration, sinusoidal congestion and inflammatory cell infiltration were observed in saline-treated sepsis group, while parenchymal degeneration, congestion and Kupffer cell activation were mild in ET+Cand NPW-treated sepsis groups. Similarly, severe degeneration of renal corpuscles and tubules with glomerular and interstitial congestion in the saline-treated sepsis group was replaced by moderate glomerular and interstitial vascular congestion and mild tubular congestion in both NPW- and ET+C-treated groups. Conclusion: NPW, applied during the first 24 hours of sepsis, exerted a dose-dependent protective effect against hepatorenal damage, which appears to involve an inhibitor
  • PublicationOpen Access
    Cerrahi menopoz oluşturulmuş sıçanların karaciğer ve böbrek dokularında oksidan/antioksidan dengenin korunmasında egzersizin ve östrojenin yararlı etkileri
    (2022-09-01) YÜKSEL, MERAL; ERCAN, FERİHA; YILDIRIM, ALPER; YEGEN, BERRAK; Tamer S. A. , Levent N., Yüksel M., Ercan F., Yıldırım A., Yegen B.
    Amaç: Bu çalışmanın amacı cerrahi olarak menopoz oluşturulan sıçanların böbrek ve karaciğerlerinde gözlenen histopatolojik ve fonksiyonel değişiklikleri ve östrojen veya egzersizin ya da östrojen-egzersiz kombinasyonunun oksidan hasar üzerine etkilerini araştırmaktır.Materyal ve Metot: Anestezi altında Sprague Dawley dişi sıçanlara (n=32) bilateral overiektomi uygulandı ve tüm sıçanlar rastgele olarak iki gruba ayrıldı. Sıçanların yarısına normal içme suyu, diğer yarısının içme sularına östrojen (1mg/kg/gün) eklendi. İki hafta sonra gruplar kendi içlerinde sedanter ve egzersiz (5 gün/hafta, 30 daki-ka, 8 hafta) gruplarına ayrıldı. Deney protokolünün sonun-da serum, karaciğer ve böbrek örnekleri biyokimyasal ve histopatolojik incelemeler için alındı. Femurda da histopa-tolojik değerlendirme yapıldı.Bulgular: Cerrahi olarak menopoz oluşturulan sıçan-larda östrojenin böbrek dokusunda nötrofil infiltrasyonunu ve reaktif oksijen türlerinin üretimini baskılayarak koruyu-cu etki gösterdiği, kemik kütlesinde hafif düzeyde artışa neden olduğu, ancak karaciğerin antioksidan glutatyon düzeyinde azalmaya yol açtığı belirlenmiştir. Buna karşın, östrojen uygulaması menopozda yapılan egzersiz nedeniy-le karaciğerde oluşan oksidan stresi engellemiştir. Egzer-sizle veya egzersize östrojen tedavisinin eklenmesiyle böbrek fonksiyonları önemli ölçüde etkilenmezken, kemik yapısında tek başına östrojene kıyasla daha olumlu deği-şiklikler gözlenmiştir.Sonuç: Östrojen replasmanı kemik dokusundaki olum-lu etkilerinin yanı sıra karaciğer ve böbrekte oksidan stresi azaltmakta ve özellikle karaciğerde egzersize bağlı gelişen oksidan stresi baskılayarak koruyucu etki göstermektedir.
  • PublicationOpen Access
    Nikotinin Sıçan Pankreatit_x000D_ Modelindeki Hafifletici Etkisinde_x000D_ Vagusun Rolünün Araştırılması
    (2021-04-01) YEGEN, BERRAK; Meltem KOLGAZİ;Zozan GÜLEKEN;Bircan KOLBAŞI;Canberk Sami BAŞIBÜYÜK;Feriha ERCAN;Berrak Çağlayan YEĞEN
    Nikotinin birçok farklı dokuda anti-inflamatuvar etkilere sahip olduğu ve bu etkileri kolinerjik anti-inflamatuvar yolağı aktive_x000D_ ederek gerçekleştirdiği gösterilmiştir. Çalışmada akut pankreatit modelinde nikotin tedavisinin etkilerini ve bu etkilerin_x000D_ kolinerjik yolla ilişkisini araştırmak amaçlanmıştır. Wistar albino sıçanların pankreas-safra ortak kanalı bağlanırken (PSKB),bir_x000D_ gruba da yalancı-cerrahi (YC) uygulandı. PSKB sıçanlara vagal aferent denervasyon (perivagal kapsaisin; 10mg/ml) veya_x000D_ trunkal vagotomi uygulandı ya da vagusları sağlam bırakıldı. PSKB grupları cerrahi sonrası ikiye ayrılarak 4 gün boyunca_x000D_ intraperitoneal nikotin (1 mg/kg/gün) ya da serum fizyolojik verildi. Dördüncü günde dekapitasyonu takiben, serumda tümör_x000D_ nekroz faktör (TNF)-∝ ve interlökin (IL)-10 ölçümü, akciğer, karaciğer ve pankreas dokularında miyeloperoksidaz aktivitesi_x000D_ (MPO), malondialdehit (MDA), glutatyon (GSH) ölçümleri ve histolojik inceleme yapıldı. TNF-∝ düzeyi PSKB grubunda YC_x000D_ grubuna göre belirgin şekilde daha yüksekken, nikotin tedavisi alanlarda belirgin şekilde daha düşüktü. IL-10 düzeyi ise SF_x000D_ tedavisi almış PSKB grubunda YC grubuna göre daha düşüktü ve nikotin tedavisi ile arttığı gözlendi.YC grubuna göre PSKB_x000D_ grubunun pankreas, karaciğer ve akciğer dokularında mikroskopik hasar, MDA, MPO düzeyleri artarken GSH düzeyleri azaldı._x000D_ Nikotin tedavisi ile karaciğer ve pankreas dokularındaki hasar, MDA, MPO düzeyleri azaldı ve GSH miktarları korundu. Vagal_x000D_ aferent denervasyon ya da trunkal vagotomi yapılması nikotinin bu koruyucu etkilerini değiştirmedi. Sonuçlar, nikotinin_x000D_ pankreatit hasarına karşı koruyucu etkilerini vagal yoldan bağımsız olarak, doğrudan immün hücreler üzerindeki ∝7nAChR_x000D_ aktivasyonu ile nötrofil infiltrasyonunu ve pro-inflamatuvar sitokinleri inhibe ederek gerçekleştirdiğini ortaya koymaktadır._x000D_ _x000D_ Anahtar Kelimeler: pankreatit, nikotin, vagus, inflamasyon, pankreatik kanal bağlama
  • PublicationOpen Access
    Antioxidant and neuroprotective effects of dexpanthenol in rats induced with traumatic brain injury
    (2023-02-12) YEGEN, BERRAK; Kuru Bektaşoğlu P., Koyuncuoğlu T., Özaydın D., Kandemir C., Akakın D., Yüksel M., Gürer B., Çelikoğlu E., Yeğen B.
    Trauma-induced primary damage is followed by secondary damage, exacerbating traumatic brain injury (TBI). Dexpanthenol has been shown to protect tissues against oxidative damage in various inflammation models. This study aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI. Wistar albino male rats were randomly assigned to control (n = 16), trauma (n = 16) and dexpanthenol (500 mg/kg; n = 14) groups. TBI was induced under anesthesia by dropping a 300 g weight from 70-cm height onto the skulls of the rats. Twenty-four hours after the trauma, the rats were decapitated and myeloperoxidase (MPO) levels, luminol- and lucigenin-enhanced chemiluminescence (CL), malondialdehyde (MDA) levels, superoxide dismutase (SOD) levels, and catalase (CAT) and caspase-3 activities were measured in brain tissues. Following transcardiac paraformaldehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. In the trauma group, MPO level, caspase-3 activity and luminol-lucigenin CL levels were elevated (p < 0.05–0.001) when compared to controls; meanwhile in the dexpanthenol group these increases were not seen (p < 0.05–0.001) and MDA levels were decreased (p < 0.05). Decreased SOD and CAT activities (p < 0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol group (p < 0.05–0.001). in the dexpanthenol group there was relatively less neuronal damage observed microscopically in the cortices after TBI. Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI.