Person: YEGEN, BERRAK
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YEGEN
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BERRAK
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Publication Metadata only Nesfatin-1 ameliorates oxidative bowel injury in rats with necrotizing enterocolitis: The role of the microbiota composition and claudin-3 expression(W B SAUNDERS CO-ELSEVIER INC, 2020) YEGEN, BERRAK; Cerit, Kivilcim Karadeniz; Koyuncuoglu, Turkan; Yagmur, Damla; Eyuboglu, Irem Peker; Sirvanci, Serap; Akkiprik, Mustafa; Aksu, Burak; Dagli, E. Tolga; Yegen, Berrak C.Background and Purpose: Ongoing high mortality due to necrotizing enterocolitis (NEC) necessitates the investigation of novel treatments to improve the outcome of the affected newborns. The aim was to elucidate the potential therapeutic impact of the nesfatin-1, a peptide with anti-inflammatory and anti-apoptotic effects in several inflammatory processes, on NEC-induced newborn rats. Materials and Methods: Sprague-Dawley pups were separated from their mothers, fed with a hyperosmolar formula and exposed to hypoxia, while control pups had no intervention. NEC-induced pups received saline or nesfatin-1 (0.2 mu g/kg/day) for 3 days, while some nesfatin-1 treated pups were injected with capsaicin (50 mu g/g) for the chemical ablation of afferent neurons. On the 4th day, clinical state and macroscopic gut assessments were made. In intestines, immunohistochemical staining of cycloxygenase-2 (COX-2), nuclear factor (NF)-kappa B-p65 (RelA), vascular endothelial growth factor (VEGF), claudin-3 and zonula occludens-1 (ZO-1) were performed, while gene expressions of COX-2, occludin, claudin-3, NF-kappa B-p65 (RelA) and VEGF were determined using q-PCR. In fecal samples, relative abundance of bacteria was quantified by q-PCR. Biochemical evaluation of oxidant/antioxidant parameters was performed in both intestinal and cerebral tissues. Results: Claudin-3 and ZO-1 immunoreactivity scores were significantly elevated in the nesfatin-1 treated control pups. Nesfatin-1 reduced NEC-induced high macroscopic and clinical scores, inhibited NF-kappa B-65 pathway and maintained the balance of oxidant/antioxidant systems. NEC increased the abundance of Proteobacteria with a concomitant reduction in Actinobacteria and Bacteroidetes, while nesfatin-1 treatment reversed these alterations. Modulatory effects of nesfatin-1 on microbiota and oxidative injury were partially reversed by capsaicin. Immunohistochemistry demonstrated that nesfatin-1 abolished NEC-induced reduction in claudin-3. Gene expressions of COX-2, NF-kappa B, occludin and claudin-3 were elevated in saline-treated NEC pups, while these up-regulated mRNA levels were not further altered in nesfatin-1-treated NEC pups. Conclusion: Nesfatin-1 could be regarded as a potential preventive agent for the treatment of NEC. (C) 2020 Elsevier Inc. All rights reserved.Publication Metadata only Nesfatin-1 treatment preserves antioxidant status and attenuates renal fibrosis in rats with unilateral ureteral obstruction(2022-06-01) ÇETİNEL, ŞULE; YEGEN, BERRAK; KAYA, ÖZLEM TUĞÇE; ÖZBEYLİ, DİLEK; Tezcan N., Özdemir-Kumral Z. N., Yenal N. Ö., Çilingir-Kaya Ö. T., Virlan A. T., Özbeyli D., Çetinel Ş., Yeğen B., Koç M.Background Nesfatin-1 (NES-1), an anorexigenic peptide, was reported to have anti-inflammatory and anti-apoptotic actions in several inflammation models. Methods To elucidate potential renoprotective effects of NES-1, unilateral ureteral obstruction (UUO) was induced in male Sprague Dawley rats by ligating left ureters. The rats were injected intraperitoneally with either saline (SL) or NES-1 (10 mu g/kg/day) for 7 or 14 days (n = 8 in each group). On the 7th or 14th day, obstructed kidneys were removed for the isolation of leucocytes for flow-cytometric analysis and the assessments of biochemical and histopathological changes. Results Opposite to glutathione levels, renal myeloperoxidase activity in the SL-treated UUO group was significantly increased compared with the sham-operated group, while NES-1 treatment abolished the elevation. The percentages of CD8+/CD4+ T-lymphocytes infiltrating the obstructed kidneys were increased in the SL-treated groups but treatment with NES-1 did not prevent lymphocyte infiltration. Elevated tumour necrosis factor-alpha (TNF-alpha) levels in SL-treated UUO group were decreased with NES-1. Although total degeneration scores were similarly increased in all UUO groups, tubular dilatation scores were significantly increased in UUO groups and lowered by NES-1 only in the 7-day treated group. Elevated interstitial fibrosis scores in the SL-treated groups were decreased in both 7- and 14-day NES-1 treated groups, while alpha-smooth muscle actin (alpha-SMA) and apoptosis scores were depressed in both NES-1 treated groups. Conclusion The present data demonstrate that UUO-induced renal fibrosis is ameliorated by NES-1, which appears to involve the inhibition of neutrophil infiltration and thereby amelioration of oxidative stress and inflammation. These data suggest that NES-1 may have a regulatory role in protecting the kidneys against obstruction-induced renal injury.Publication Metadata only NICARDIPINE REDUCES THE LEVELS OF LEUKOTRIENE-C4 AND PROSTAGLANDIN-E2, FOLLOWING DIFFERENT ISCHEMIC PERIODS IN RAT-BRAIN TISSUE(CHURCHILL LIVINGSTONE, 1992) YEGEN, BERRAK; AKTAN, S; AYKUT, C; OKTAY, S; YEGEN, B; ERCAN, SIschemic depolarization of nerve membranes is associated with a rapid influx of calcium into the cell, resulting in production of arachidonic acid (AA) metabolites. These metabolites, particularly leukotriene C4 (LTC4) have a very potent vasoconstrictor effect on cerebral arteries inducing vasogenic edema that may damage the ischemic penumbra. Calcium antagonists are assumed to prevent or reduce metabolic disturbances associated with ischemia. In this study, after developing an experimental animal model simulating the concept of the ischemic penumbra in the rat, the levels of LTC4 and prostaglandin E2 (PGE2) produced in the forebrain following different ischemic periods, such as 4th, 15th, 60th and 240th min were measured by a bioassay method, including 6 rats for each ischemic group. Then the effect of the 1-4 dihydropirine nicardipine (1 mg/kg) on these mediators was investigated by giving it to the rat 30 min before the development of the ischemic model in each corresponding group (n = 6). We showed that nicardipine significantly reduced the high levels of LTC4 and PGE2 in the 4th min and 4th h of cerebral ischemia (p < 0.005, p < 0.0005). So it may be concluded that institution of nicardipine may be helpful in protecting the ischemic penumbra during the early hours of cerebral ischemia.Publication Metadata only Melatonin protects against oxidative organ injury in a rat model of sepsis(SPRINGER, 2005) YEGEN, BERRAK; Sener, G; Toklu, H; Kapucu, C; Ercan, F; Erkanli, G; Kacmaz, A; Tilki, M; Yegen, BCPurpose. Based on the potent antioxidant effects of melatonin, we investigated the putative protective role of melatonin against sepsis-induced oxidative organ damage in rats. Methods. Sepsis was induced by cecal ligation and puncture (CLP) in Wistar albino rats. Animals subjected to CLP and sham-operated control rats were given saline or melatonin 10 mg/kg intraperitoneally 30 min before and 6 h after the operation. The rats were killed 16 h after the operation and the biochemical changes were investigated in the liver, kidney, heart, lung, diaphragm, and brain tissues by examining malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. We also examined the tissues microscopically. Results. Sepsis resulted in a significant decrease in GSH levels and a significant increase in MDA levels and MPO activity (P < 0.05-P < 0.001) showing oxidative damage, which was confirmed by histological examination. Melatonin clearly reversed these oxidant responses and the microscopic damage, demonstrating its protective effects against sepsis-induced oxidative organ injury. Conclusion. The increase in MDA levels and MPO activity and the concomitant decrease in GSH levels demonstrate the role of oxidative mechanisms in sepsis-induced tissue damage. Melatonin, by its free radical scavenging and antioxidant properties, ameliorated oxidative organ injury. Thus, supplementing antiseptic shock treatment with melatonin may be beneficial in the clinical setting.Publication Metadata only Leukotriene receptor blocker montelukast protects against burn-induced oxidative injury of the skin and remote organs(ELSEVIER SCI LTD, 2005) YEGEN, BERRAK; Sener, G; Kabasakal, L; Cetinel, S; Contuk, G; Gedik, N; Yeken, BCThermal injury elicits several systemic consequences, among them the systemic inflammatory response where the generation of reactive oxygen radicals and lipid peroxidation play important roles. In the present study, we investigated whether the leukotriene receptor blocker montelukast is protective against burn-induced remote organ injury. Under brief ether anaesthesia, shaved dorsum of the rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10 s. Montelukast (10 mg/kg) or saline was administered intraperitoneally immediately after and at the 12th hour of the burn injury. Rats were decapitated 24 h after burn injury and the tissue samples from lung, liver, kidney and skin were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Tissues were also examined microscopically. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels and creatinine, urea (BUN) concentrations were determined to assess liver and kidney function, respectively. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) were also assayed in serum samples. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the burn group as compared to control group. On the other hand, montelukast treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by thermal trauma. Findings of the present study suggest that montelukast possesses an anti-inflammatory effect on burn-induced damage in remote organs and protects against oxidative organ damage by a neutrophil-dependent mechanism. (C) 2005 Elsevier Ltd and ISBI. All rights reserved.Publication Metadata only GASTRIC LIPID-PEROXIDATION, GLUTATHIONE AND CALCIUM-CHANNEL BLOCKERS IN THE STRESS-INDUCED ULCER MODEL IN RATS(ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD, 1994) YEGEN, BERRAK; ALICAN, I; TOKER, F; ARBAK, S; YEGEN, BC; YALCIN, AS; OKTAY, SThe antiulcer activity of verapamil and its analogues devapamil and gallopamil was studied. All three drugs reduced cold-restraint stress-induced ulcer development. Gallopamil almost abolished gastric ulcers. Verapamil prevented the increase in gastric lipid peroxidation (LP) due to stress. On the other hand, devapamil and gallopamil increased gastric lipid peroxidation and decreased glutathione levels. This effect may be attributed to the increase in oxygen supply due to possible effective vasodilation at gastric mucosa. The second part of this study revealed that stress-induced gastric ulcers in rats rapidly and spontaneously heal and disappear within 24 h. During recovery, gastric LP decreased and glutathione levels increased within 12 h after the withdrawal of stress, preceded by an initial reduction in glutathione. After 72 h, an unexplained increase in gastric LP and a decrease in glutathione were observed. Treatment with verapamil, devapamil and gallopamil promoted healing, gallopamil being again the most effective. Their effects on gastric LP and glutathione levels are in accordance with the results of pretreatment experiments. In conclusion, devapamil and gallopamil are effective antiulcer agents against stress-induced ulcers, but unlike verapamil, antioxidant activity does not seem likely to be among their mechanisms of action.Publication Metadata only Ghrelin alleviates biliary obstruction-induced chronic hepatic injury in rats(ELSEVIER, 2008) YEGEN, BERRAK; Iseri, Sevgln Oezlem; Sener, Goeksel; Saglam, Beyhan; Ercan, Feriha; Gedik, Nursal; Yegen, Berrak C.Background: Reactive oxygen species and oxidative stress are implicated in hepatic stellate cell activation and liver fibrosis, which are initiated by recruitment of inflammatory cells and by activation of cytokines. Objective: The possible anti-oxidant and anti-inflammatory effects of ghrelin were evaluated in a hepatic fibrosis model in rats with bile duct ligation (BDL). Methods: Under anesthesia, bile ducts of Sprague Dawley rats were ligated, and half of the rats were subcutaneously administered with ghrelin (10 ng/kg/day) and the rest with saline for 28 days. Sham-operated control groups were administered saline or ghrelin. On the 28th day of the study, rats were decapitated and malondialdehyde (NIDA) content - an index of lipid peroxidation, and myeloperoxidase (MPO) activity - an index of neutrophil infiltration - were determined in the liver tissues. Oxidant-induced tissue fibrosis was determined by collagen contents, while the hepatic injury was analyzed microscopically. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels and lactate dehydrogenase (LDH) levels were determined to assess liver function and tissue damage, respectively. Pro-inflammatory cytokines; TNF-alpha, IL-1 beta and IL-6 were also assayed in plasma samples. Results: In the saline-treated BDL group, hepatic NIDA levels, MPO activity and collagen content were increased (p < 0.001), suggesting oxidative organ damage, as confirmed histologically. In the ghrelin-treated BDL group, however, all of the oxidant responses were reversed significantly (p < 0.05-p < 0.001). Serum AST, ALT, LDH levels, and cytokines were elevated in the BDL group as compared to the control group, while this increase was significantly decreased by ghrelin treatment. Conclusion: Owing to the anti-inflammatory and anti-oxidant effect as demonstrated in our study, it is possible to speculate that exogenously administered ghrelin may possess an antifibrotic effect against biliary obstruction-induced liver fibrosis. Thus, it seems likely that ghrelin may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction. (c) 2007 Elsevier B.V. All rights reserved.Publication Open Access Methimazole-induced hypothyroidism in rats ameliorates oxidative injury in experimental colitis(SOC ENDOCRINOLOGY, 2003-06-01) YEGEN, BERRAK; Isman, CA; Yegen, BC; Alican, IDepression of metabolism by hypothyroidism decreases oxidant production and thus protects tissues against oxidant damage. Moreover, it is well-known that abnormal gut motility is a common manifestation in hypo/ hyperthyroidism. In this study, we aimed to investigate the putative beneficial effects of methimazole on oxidative injury and dysmotility in a rat colitis model. Methimazole (0(.)04%) was administered in drinking water starting 15 days prior to induction of colitis. Colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid (30 mg/ml; 0(.)8 ml) in ethanol. Six days after the induction of colitis, the fecal output was measured and used as an index for colonic motility. All rats were decapitated on the seventh day. The distal colon was weighed and the mucosal lesions were scored. Colonic lipid peroxidation (LP) and glutathione (GSH) measurements were performed. The macroscopic score, the colonic wet weight and LP values of the euthyroid colitis group were found to be higher than those of the control group (P<0(.)05-0(.)001). All these parameters were reduced in the methimazole-treated colitis group (P<0(.)01-0(.)001). The decrease in colonic GSH levels in the colitis group was completely abolished in the methimazole-treated colitis rats (P<0(.)01). Induction of colitis increased the average fecal output compared with the control group (P<0(.)05) and methimazole in the colitis group exaggerated the fecal output (P<0(.)001). In conclusion, methimazole reduces colonic oxidative injury probably due to hypometabolism, which is associated with a decrease in the production of reactive oxygen intermediates and an increase in the response of antioxidant systems.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 Amelioration of sepsis-induced hepatic and ileal injury in rats by the leukotriene receptor blocker montelukast(CHURCHILL LIVINGSTONE, 2005) YEGEN, BERRAK; Sener, G; Sehirli, O; Cetinel, S; Ercan, F; Yuksel, M; Gedik, N; Yegen, BCBackground. Sepsis is a generalized inflammatory response, which involves organ systems remote from the locus of the initial infectious insult, involves the release of cytokines and the subsequent formation of reactive oxygen and nitrogen species. Objective: The aim of this study was to investigate the possible protective effect of montelukast, a leukotriene receptor blocker, against oxidative damage in the liver and ileum of septic rats. Methods: Sepsis was induced by cecal ligation and puncture method in female Wistar albino rats. Sepsis and sham operated (control) groups received either saline or montelukast (10 mg/kg, ip) immediately after the operation and at 12 h. Twenty-four hours after the surgery, rats were decapitated and malondialdehyde (MDA) content-an index of lipid peroxidation, glutathione (GSH) levels-a key antioxidant, myeloperoxidase (MPO) activity-an index of neutrophil infiltration, and collagen contents were determined in the liver and ileum. Formation of reactive oxygen species in liver and ileal tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Both tissues were also analyzed histologically. Serum lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) level were assessed in trunk blood. Results: Sepsis resulted in decreased GSH levels, and increased MDA levels, MPO activity, CL levels and collagen contents in both the liver and the ileum (P < 0.05 - P < 0.001) indicating the presence of the oxidative damage. Similarly, serum TNF-alpha and LDH were elevated in the sepsis group as compared to control group. On the other hand, montelukast treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by sepsis. Conclusion: Findings of the present study suggest that montelukast possesses an anti-inflammatory effect on sepsis-induced hepatic and intestinal damage and protects against oxidative injury by a neutrophil-dependent mechanism. (C) 2005 Elsevier Ltd. All rights reserved.
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