Person: ARABACI TAMER, SEVİL
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ARABACI TAMER
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SEVİL
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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 Open Access Neuropeptide W Exhibits Preventive and Therapeutic Effects on Acetic Acid-Induced Colitis via Modulation of the Cyclooxygenase Enzyme System(2023-01-01) ARABACI TAMER, SEVİL; ERCAN, FERİHA; YEGEN, BERRAK; ARABACI TAMER S., Akbulut S., Erdogan O., Cevik O., ERCAN F., YEGEN B.Background The novel peptide neuropeptide W (NPW) was originally shown to function in the control of feeding behavior and energy homeostasis. The aim of this study was to elucidate the putative preventive and therapeutic effects of NPW on colitis-associated oxidative injury and the underlying mechanisms for its action.Methods Sprague-Dawley rats in the acute colitis groups received NPW (0.5, 1 or 5 mu g/kg/day) injections prior to induction of colitis with acetic acid, while the chronic colitis groups were treated after the induction of colitis. In both acute and chronic colitis (CC) groups, treatments were continued for 5 days and the rats were decapitated at the 24th hour of the last injections and colon tissues were collected for assessments.Results NPW pretreatment given for 5 days before colitis induction, as well as treating rats with NPW during the 5-day course of CC, abolished colonic lipid peroxidation. NPW treatment prevented colitis-induced reduction in blood flow, diminished neutrophil infiltration, and pro-inflammatory cytokine responses. NPW pretreatment only at the higher dose reduced colonic edema and microscopic score and preserved colonic glutathione stores. Elevations in cyclooxygenase (COX) enzyme activity and COX-1 protein level during the acute phase of colitis as well as reduction in COX-2 were all reversed with NPW pretreatment. In contrast, NPW treatment was effective in reducing the elevated COX-2 concentration during the chronic phase.Conclusions NPW alleviates acetic acid-induced oxidative colonic injury in rats through the upregulation of colonic blood flow as well as the inhibition of COX-2 protein expression and pro-inflammatory cytokine production.Publication Open Access High-fat Diet Enhances Gastric Contractility, but Abolishes Nesfatin-1-induced Inhibition of Gastric Emptying(KOREAN SOC NEUROGASTROENTEROLOGY & MOTILITY, 2021-04-30) YEGEN, BERRAK; Ozdemir-Kumral, Zarife N.; Koyuncuoglu, Turkan; Arabaci-Tamer, Sevil; Cilingir-Kaya, Ozlem T.; Koroglu, Ayca K.; Yuksel, Meral; Yegen, Berrak C.Neither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND- and HFD-rats, but only lucigenin-chemiluminescence was Background/Aims Gastrointestinal motility changes contribute to development and maintenance of obesity. Nesfatin-1 (NES-1) is involved in central appetite control. The aim is to elucidate effects of NES-1 and high-fat diet (HFD) on gastrointestinal motility and to explore myenteric neuron expressions of tyrosine hydroxylase (TH), vasoactive intestinal peptide (VIP), and neuronal nitric oxide synthase (nNOS) in HFDinduced oxidative injury. Methods Sprague-Dawley rats were fed with normal diet (ND) or HFD. Gastric emptying rate was measured following NES-1 (5 pmol/rat, intracerebroventricular) preceded by subcutaneous injections of glucagon-like peptide 1 (GLP-1), cholecystokinin 1 (CCK-1), and gastrin/CCK-2 receptor antagonists. In carbachol-contracted gastric and ileal strips, contractile changes were recorded by adding NES1 (0.3 nmol/L), GLP-1, CCK-1, and gastrin/CCK-2 antagonists. Results Neither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND-and HFD-rats, but only lucigenin-chemiluminescence was increased in HFD-rats. Vasoactive intestinal peptide (VIP) and TH immunoreactivities were depressed and nNOS immunoreactivity was increased in gastric tissues of HFD-rats, while VIP and TH were enhanced, but nNOS was reduced in their intestines. Conclusions HFD caused mild systemic inflammation, disrupted enteric innervation, enhanced gastric contractility, inhibited ileal contractility, and eliminated inhibitory effect of NES-1 on gastric motility. (J Neurogastroenterol Motil 2021;27:265-278)Publication Metadata only Nesfatin-1 ameliorates testicular injury and supports gonadal function in rats induced with testis torsion(ELSEVIER SCIENCE INC, 2018) YILDIRIM, ALPER; Tamer, Sevil Arabaci; Yildirim, Alper; Koroglu, M. Kutay; Cevik, Ozge; Ercan, Feriha; Yegen, Berrak C.Testicular torsion causes ischemia-reperfusion injury and an increased risk of infertility. Nesfatin-1 is a novel peptide with antioxidant, anti-inflammatory and anti-apoptotic properties. In the present study, we aimed to investigate the putative beneficial effects of nesfatin-1 on oxidative injury and impaired testicular function induced by testis torsion. Under anesthesia, male Sprague-Dawley rats (180-230 g; n = 24) had sham-operation or they underwent testicular torsion by rotating the left testis 720 degrees and fixing it for 2 h, followed by a 2-h detorsion. Rats in each group were treated intraperitoneally with either nesfatin-1 (0.3 mu g/kg) or saline prior to the torsion or sham-torsion. At the end of the 4-h experimental period, tissue samples were removed for evaluation of spermatozoa, molecular and histochemical analyses. In saline-treated torsion/detorsion group, a high percentage of abnormal spermatozoa with head defects was observed, which was abolished in nesfatin-1 -treated torsion/detorsion group. The levels of 8-OHdG, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, caspase-3 were increased in the saline-treated torsion/detorsion group as compared to sham-operated group, while nesfatin-1 pre-treatment significantly decreased the expressions of the pro-inflammatory cytokines, depressed apoptosis, and also reduced the tubular degeneration. In addition, nesfatin-1 in torsion/detorsion group elevated expressions of transforming growth factor (TGF)-beta and reduced expressions of protein kinase B (AKT) and cAMP response element binding protein (CREB) in the testis tissue. The present findings show that nesfatin-1, by regulating AKT and CREB signaling pathways and pro-inflammatory/anti-inflammatory cytokine balance, preserves the spermatogenic cells and ameliorates torsion-detorsion-induced tubular degeneration.Publication Open Access Nesfatin-1 ameliorates oxidative brain damage and memory impairment in rats induced with a single acute epileptic seizure(2022-04-01) ARABACI TAMER, SEVİL; KOYUNCUOĞLU, TÜRKAN; AKAKIN, DİLEK; YÜKSEL, MERAL; YEGEN, BERRAK; Arabacı Tamer S., Koyuncuoğlu T., Karagöz Köroğlu A., AKAKIN D., YÜKSEL M., YEGEN B.© 2022Aims: We aimed to investigate putative neuroprotective effects of nesfatin-1 on oxidative brain injury and memory dysfunction induced by a single epileptic seizure and to compare these effects with those of antiepileptic phenytoin. Main methods: Wistar albino rats were randomly divided into a control group and pentylenetetrazole (PTZ)-seizure groups pretreated intraperitoneally (ip) with saline or nesfatin-1 (NES-1; 0.3, 1 or 3 μg/kg/day) or phenytoin (PHE; 40 mg/kg/day) or PHE + NES-1 (0.3 μg/kg/day) at 30 min before the single-dose PTZ injection (45 mg/kg; ip). All treatments were repeated at the 24th and 48th h of the provoked epileptic seizure. Passive-avoidance test was performed to assess memory function. The rats were decapitated at the 72nd hour of seizures and brain tissues were analyzed for histopathological changes and for measuring levels of malondialdehyde, glutathione, myeloperoxidase activity and reactive oxygen/nitrogen species. Key findings: In parallel to the effects of phenytoin, NES-1 reduced seizure score, elevated antioxidant glutathione content, depressed generation of nitric oxide and protected against seizure-induced neuronal damage. Additionally, increased malondialdehyde levels and elevated glial fibrillary acidic protein immunoreactivity in the cortex and hippocampus were decreased and memory dysfunction was improved by NES-1. However, NES-1 had no impact on myeloperoxidase activity or production of reactive oxygen species in the brain. Significance: The findings of the present study demonstrate that nesfatin-1 treatment provides neuroprotection against seizure-induced oxidative damage and memory dysfunction by inhibiting reactive nitrogen species and upregulating antioxidant capacity, indicating its potential in alleviating memory deficits and increasing the effectiveness of conventional anti-convulsant therapies.Publication Metadata only Treatment with estrogen receptor agonist ER beta improves torsion-induced oxidative testis injury in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2019) YILDIRIM, ALPER; Tamer, Sevil Arabaci; Yildirim, Alper; Arabaci, Sule; Ciftci, Selin; Akin, Sena; Sari, Elif; Koroglu, M. Kutay; Ercan, Feriha; Yuksel, Meral; Cevik, Ozge; Yegen, Berrak C.Aims: The purpose of the present study was to investigate the potential antioxidant, anti-apoptotic and sperm function-preserving effects of estrogen, estrogen receptor (ER) a and ER beta agonists in a rat model of testis torsion-detorsion (T/D). Main methods: Under anesthesia, 6-8-week-old male Sprague-Dawley rats underwent sham-operation or testicular torsion by fixing left testis rotated at 720 degrees for 2 h. After detorsion, rats were treated with ER alpha agonist (1 mg/kg/day, subcutaneously, sc) or ER beta agonist (1 mg/kg/day, sc) or estradiol (E-2, 1 mg/kg/day, in drinking water) or vehicle on the following two days. On the third day, testicular blood-flow was recorded and then left testes were extracted for molecular and histochemical analysis. Key findings: The findings showed that reduced testicular blood-flow following torsion was partially restored on the 3rd day of detorsion, while treatments with either of the ER agonists or E-2 returned blood flow fully back to the control levels. When the testis-torsioned rats were given ER beta agonist during the detorsion period, tubular injury was lessened, sperm count and motility were increased, while the production of reactive oxygen meta-bolites and apoptosis in the testis tissues were totally suppressed. Although a down-regulated expression of androgen receptor (AR) along with a reduction in serum testosterone level was observed in the vehicle-treated T/D group, all three treatments up-regulated the expressions of AR and its mRNA, while ER alpha agonist and E-2 suppressed the testosterone level. Significance: ER beta receptor activation during the post-ischemic period may be beneficial in protection against torsion-related oxidant testicular injury and infertility.