Person: YEGEN, BERRAK
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YEGEN
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BERRAK
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Publication Metadata only The antifibrotic drug halofuginone reduces ischemia/reperfusion-induced oxidative renal damage in rats(ELSEVIER SCI LTD, 2013) YEGEN, BERRAK; Cerit, Kivilcim Karadeniz; Karakoyun, Berna; Yuksel, Meral; Ozkan, Naziye; Cetinel, Sule; Dagli, E. Tolga; Yegen, Berrak C.; Tugtepe, HalilAim: The objective of the present study was to evaluate the protective effects of halofuginone against renal ischemia/reperfusion (I/R) injury. Materials and methods: Male Wistar albino rats were unilaterally nephrectomized and the left renal pedicles were occluded for 45 min to induce ischemia and then reperfused for 6 h (early) or for 72 h (late). The rats were treated intraperitoneally with either halofuginone (100 mu g/kg/day) or saline 30 min prior to ischemia and the dose was repeated in the late reperfusion groups. In the sham groups, rats underwent unilateral nephrectomy and were treated at similar time points. The animals were decapitated at either 6 h or 72 h of reperfusion and trunk blood and kidney samples were obtained. Results: I/R injury increased renal malondialdehyde levels, myeloperoxidase activity and reactive oxygen radical levels, and decreased the renal glutathione content. Halofuginone treatment was found to reduce oxidative I/R injury and improve renal function in the rat kidney, as evidenced by reduced generation of reactive oxygen species, depressed lipid peroxidation and myeloperoxidase activity, and increased glutathione levels. Conclusions: The present findings demonstrate the anti-inflammatory and antioxidant effects of halofuginone in renal I/R injury, supporting its potential use where renal I/R injury is inevitable. (C) 2012 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.Publication Metadata only Estrogen Protects against Oxidative Multiorgan Damage in Rats with Chronic Renal Failure(TAYLOR & FRANCIS LTD, 2009) YEGEN, BERRAK; Kasimay, Oezguer; Sener, Goeksel; Cakir, Baris; Yueksel, Meral; Cetinel, Sule; Contuk, Gazi; Yegen, Berrak C.The impact of sex dimorphism on chronic renal failure (CRF)-induced oxidative multiorgan damage and the effects of estradiol (E-2) loss and E-2 supplementation on the progress of CRF were studied. Sprague-Dawley rats underwent 5/6 nephrectomy (CRF), and a group of female rats had bilateral ovariectomy (OVX), while the sham-operated rats had no nephrectomy or OVX. Rats received either estradiol propionate (50 mu g/kg/day) or vehicle for six weeks. Serum BUN levels were elevated in both male and female CRF groups treated with vehicle, while creatinine level was not significantly changed in the female CRF group. CRF-induced elevation in serum TNF-alpha of male rats was abolished when the animals were treated with E-2, while OVX exaggerated TNF-alpha response. In OVX and male rats with CRF, E-2 treatment reversed the malondialdehyde elevations in all the studied tissues (kidney, heart, lung, ileum, brain, liver, and gastrocnemius muscle), while depletion of glutathione in these tissues was prevented by E-2 treatment. Similarly, increased levels of myeloperoxidase activity, lucigenin chemiluminescence, and collagen in most of the tissues were reversed by E-2 treatment. The findings show that the extent of tissue injuries was relatively less in females, while ovariectomy exacerbated all the indices of oxidative injury. Moreover, the administration of E-2, with its potent anti-oxidant and anti-inflammatory effects, markedly improved CRF-induced systemic inflammatory outcomes in both male and female rats by depressing tissue neutrophil infiltration and modulating the release of inflammatory cytokines.Publication Metadata only The ameliorative effects of melatonin on acetic acid-induced gastric ulcer in rats via its modulatory effects on gut microbiota(CUKUROVA UNIV, FAC MEDICINE, 2021) YILDIRIM, ALPER; Tamer, Sevil Arabaci; Yildirim, Alper; Cevik, Ozge; Aksu, Burak; Yuksel, Meral; Dertsiz, Ekin Kuntsal; Sirvanci, Serap; Yegen, Berrak C.Purpose: The aim of this study was of observe the possible protective effects of melatonin pretreatment on oxidative damage and microbiota alteration due to gastric ulcer in rats. Materials and Methods: Wistar-albino rats were given (n=32) melatonin (4 mg/kg/day), antibiotic mixture (AB; 1g/L ampicillin + 1g/L neomycin + 1g/L metronidazole), melatonin+AB in drinking water for 12 days or tap water for 15 days (control group; n=8). Subsequently, ulcer was induced. All treatments were continued for three days. Gastric tissues were obtained for biochemical and histopathological examinations, and fecal samples from the rectum were stored for bacteriological measurements. Results: MPO and MDA levels were increased in untreated ulcer groups compared to the control group. In addition, the levels of luminol-lucigenin chemiluminescence (CL) and 8-OHdG and TNF-alpha and IL-8 protein expressions were also increased, while TNF-alpha, IL-8, MDA, 8-OHdG, luminol and lucigenin CL levels were significantly decreased in the melatonin-treated ulcer groups. However, melatonin+AB pretreatment increased antioxidant GSH levels and anti-inflammatory IL-10 levels, and suppressed caspase-3 activity and reduced MPO back to control level. Conclusion: We anticipate that melatonin treatment, which is an effective antioxidant and radical scavenger, can accelerate ulcer healing along with antibiotics and increase the variety of bacteria impaired by antibiotics in the colon.Publication Metadata only The protective effect of oxytocin on renal ischemia/reperfusion injury in rats(ELSEVIER SCIENCE BV, 2007) YEGEN, BERRAK; Tugtepe, Halil; Sener, Goksel; Biyikli, Nese Karaaslan; Yuksel, Meral; Cetinel, Sule; Gedik, Nursal; Yegen, Berrak C.Aim: Oxytocin was previously shown to have anti-inflammatory effects in different inflammation models. The major objective of the present study was to evaluate the protective role of oxytocin (OT) in protecting the kidney against ischemia/reperfusion (I/R) injury. Materials and methods: Male Wistar albino rats (250-300 g) were unilaterally nephrectornized, and subjected to 45 min of renal pedicle occlusion followed by 6 It of reperfusion. OT (1 mg/kg, ip) or vehicle was administered 15 min prior to ischemia and was repeated immediately before the reperfusion period. At the end of the reperfusion period, rats were decapitated and kidney samples were taken for histological examination or determination of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Creatinine and urea concentrations in blood were measured for the evaluation of renal function, while TNF-alpha and lactate dehydrogenase (LDH) levels were determined to evaluate generalized tissue damage. Formation of reactive oxygen species in renal tissue samples was monitored by chemiluminescence technique using luminol and lucigenin probes. Results: The results revealed that I/R injury increased (p < 0.01-0.001) serum urea, creatinine, TNF-alpha and LDH levels, as well as MDA, MPO and reactive oxygen radical levels in the renal tissue, while decreasing renal GSH content. However, alterations in these biochemical and histopathological indices due to l/R injury were attenuated by OT treatment (P < 0.05-0.001). Conclusions: Since OT administration improved renal function and microscopic damage, along with the alleviation of oxidant tissue responses, it appears that oxytocin protects renal tissue against I/R-induced oxidative damage. (c) 2006 Elsevier B.V. All rights reserved.Publication Metadata only 83: phoenixin-14 ameliorates cholestatic liver injury and bileinduced acute pancreatic injury in rats(2022-05-01) KAHRAMAN, MERVE MERİÇ; YÜKSEL, MERAL; YEGEN, BERRAK; ERCAN, FERİHA; Şen L. S. , Kahraman M. M. , Mermer K. S. , Köroğlu K., Yüksel M., İmeryüz N., Ercan F., Yegen B.Background: Bile duct obstruction, which results in cholestatic liver injury, is also the major cause of acute pancreatitis. Phoenixin (PNX) was originally defined as a hypothalamic peptide associated with a wide range of physiological processes and exerts antioxidant and antiinflammatory effects. PNX is expressed in several peripheral organs including pancreas and liver. We aimed to evaluate possible therapeutic effects of PNX on hepatic and pancreatic damage induced by biliary or pancreaticobiliary duct obstruction. Methods: In male Sprague Dawley rats, bile duct ligation (BDL; n=16) or pancreaticobiliary duct ligation (PBDL; n= 16) was performed under ketamine anesthesia, while control rats (n=8) had sham-surgery. Either PNX-14 (50 µg/kg/day) or saline was subcutaneously injected immediately after surgery and in the following 2 days. On the post-operative 3rd day, hepatic and renal blood flow was measured using laser Doppler flowmeter under anesthesia and the rats were then euthanized. In the liver and pancreas samples, levels of malondialdehyde, antioxidant glutathione and myeloperoxidase activity were measured by spectrophotometry, while luminol- and lucigenin-enhanced chemiluminescence (CL) levels were measured to assess formation of reactive oxygen species (ROS). Tissue samples were stained by hematoxylin-eosin to calculate microscopic damage scores. Statistical analyses were made by one-way ANOVA. Results: Increased microscopic damage scores in the pancreas of saline-treated PBDL (p<0.001) and in the liver of saline-treated BDL group (p<0.001) were reduced by PNX14 treatment (p<0.01), but PBDL-induced hepatic damage (p<0.001) was not changed by PNX-14. Pancreatic and hepatic levels of malondialdehyde and myeloperoxidase activity and pancreatic glutathione levels were not different among the experimental groups, while hepatic glutathione level was elevated in PNX-14-treated BDL (p<0.001) and PBDL (p<0.01) groups as compared to control group. Despite a non-significant fall in renal or hepatic blood flow in saline-treated BDL rats, PBDL significantly reduced hepatic (p<0.001) and renal (p<0.01) blood flow, while PNX-14 reversed blood flow in both organs back to control levels (p<0.05). The CL levels of luminol and lucigenin were increased in both hepatic and pancreatic tissues of saline-treated BDL and PBDL groups (p<0.05-0.001), showing enhanced ROS generation. However, CL levels in both the liver and pancreas of PNX-14-treated BDL and PBDL groups were significantly reduced as compared to those measured in the liver and pancreas of respective saline-treated groups (p<0.05-0.001). Conclusion: In conclusion, cholestatic liver injury and bile-induced pancreatic injury are alleviated by PNX-14 treatment, which appears to act via its ROS scavenging activity, by replenishing hepatic antioxidant capacity and restoring impaired organ perfusion.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 Halofuginone, a Specific Inhibitor of Collagen Type 1 Synthesis, Ameliorates Oxidant Colonic Damage in Rats with Experimental Colitis(SPRINGER, 2010) YEGEN, BERRAK; Karakoyun, Berna; Yuksel, Meral; Ercan, Feriha; Salva, Emine; Isik, Isil; Yegen, Berrak C.To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 mu g/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.Publication Metadata only Stimulation of estrogen receptors attenuates oxidant skin injury in hyperglycemic rats with incisional wound(2023-01-01) KAHRAMAN, MERVE MERİÇ; YÜKSEL, MERAL; ERCAN, FERİHA; YEGEN, BERRAK; Sen L. S., Akgun T., KAHRAMAN M. M., YÜKSEL M., ERCAN F., YEGEN B.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.
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