Person: ARABACI TAMER, SEVİL
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ARABACI TAMER
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SEVİL
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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 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.