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ERTAŞ, BÜŞRA

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2018 - 20203
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Author: ŞENER, GÖKSEL × Subject: EXPRESSION ×

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Now showing 1 - 3 of 3
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    Mesenchymal stem cell therapy improves erectile dysfunction in experimental spinal cord injury
    (SPRINGERNATURE, 2020) ERTAŞ, BÜŞRA; Albayrak, Omercan; Sener, Tarik Emre; Ersahin, Mehmet; Ozbas-Turan, Suna; Ekentok, Ceyda; Tavukcu, Hasan Huseyin; Cevik, Ozge; Cetinel, Sule; Ertas, Blisra; Sener, Goksel
    The aim of this study is to investigate the therapeutic potential of adipose-derived mesenchymal stem cell (AD-MSC) from brown adipose tissue on erectile dysfunction (ED) in experimentally induced spinal cord injury in rats. 24 male Wistar rats were divided into 3 groups; control, spinal cord injury (SCI) + vehicle, and SCI + AD-MSC. To induce SCI, a standard weight-drop method that induced a moderate to severe injury (100 g/cm force) at T7-T10, was used. AD-MSC (3 x 105 cells /5 mu L) was applied by local transplantation into the region of injury. At the end of four-weeks, rats underwent neurological examinations and then intracavernosal and mean arterial pressures (ICP and MAP) measurements. After decapitation, spinal cord and cavernosal tissue samples were taken to analyze neuronal nitric oxide synthase (n-NOS), proto-oncogene protein c-FOS and nerve growth factor (NGF). Tissues were also examined histologically. Spinal cord injury caused decrease on NGF and n-NOS levels while c-FOS was increased. The ICP/MAP value in vehicle-treated SCI rats was found to be significantly higher than the control group. On the other hand, in SCI + AD-MSC group, all these parameters were reversed back to control levels. AD-MSC therapy may be beneficial against erectile dysfunction in experimentally induced SCI by ameliorating neuronal damage.
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    Nicorandil preserves blood-brain barrier and improves memory impairment in hypertensive rats
    (MARMARA UNIV, 2019-11-15) YEGEN, BERRAK; Cevikelli Yakut, Zatiye Ayca; Ertas, Busra; Koyuncuoglu, Turkan; Yegen, Berrak C.; Sener, Goksel
    In renovascular hypertension (RVH), oxidative stress and inflammation due to high blood pressure and elevated levels of angiotensin 2 are mainly responsible of cerebrovascular complications and impaired cognitive functions. Since the nicorandil has been shown to exert neuroprotective, anti-inflammatory and antioxidant effects, we investigated the effect of nicorandil against vascular dementia and blood brain barrier damage in a rat model of angiotensin-dependent hypertension. Wistar albino rats, were divided as sham-operated control, renovascular hypertension (RVH) and Nicorandil-treated RVH groups. Silver clip was implanted onto the left renal artery. Using the tail-cuff method, blood pressure of rats was measured before the surgery and at the end of the post-surgical 3rd and 12th weeks. Nicorandil (4mg/kg, orally) or vehicle was administered for 9 weeks. Twelve weeks after RVH surgery, a new object recognition test was performed. Following the determination of blood brain barrier integrity, serum samples were taken for the evaluation of proinflammatory cytokines tumor necrosis alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Levels of sodium-potassium adenosine triphosphatase (Na+/K+-ATPase), as a marker of endothelial damage, were evaluated in the hippocampal tissues. RVH resulted in significant increases in TNF-alpha and IL-1 beta levels and decreases in Na+/K+-ATPase levels, along with impairment in blood brain barrier integrity and memory performance. In the nicorandil treatment group, these indices were reversed back to control levels. The present data demonstrated that nicorandil attenuates RVH-induced memory impairment and blood brain barrier damage in rats with RVH.
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    Ameliorative effects of riboflavin on acetic acid-induced colonic injury in rats
    (WILEY, 2018) ERTAŞ, BÜŞRA; Karakoyun, Berna; Ertas, Busra; Yuksel, Meral; Akakin, Dilek; Cevik, Ozge; Sener, Goksel
    Riboflavin (RF) has been found to be a promising antioxidant and/or anti-inflammatory agent in several studies. However, the effect of RF against acetic acid (AA)-induced colonic injury is currently unknown. This study aimed to investigate the potential antioxidant and protective effects of RF in a rat model of ulcerative colitis. Starting immediately after the colitis induction (AA+RF group) or 1week before the colitis induction (RF+AA+RF group), the rats were treated with RF (25mg/kg per day; p.o.) for 3days. The control and AA groups received saline (1mL; p.o.) whereas AA+SS group (positive control) received sulfasalazine (100mg/kg per day; p.o.) for 3days. Colonic samples were taken for the biochemical and histological assessments on the third day. High damage scores, elevated tissue wet weight index (WI), tissue myeloperoxidase (MPO) activity, 8-hydroxy-2-deoxyguanosine levels and chemiluminescence values, and a pronounced decrease in antioxidant glutathione (GSH) levels of the AA group were all reversed by RF pretreatment (RF+AA+RF group) and SS treatment (AA+SS group) (P<.05-.001). Tissue WI, MPO activity and GSH levels were not statistically changed in the AA+RF group. Western blot analysis revealed that the decreased protein expressions of tissue collagen (COL) 1A1, COL3A1 and transforming growth factor-1 in the AA group were elevated in all the treatment groups (P<.05-.001). In conclusion, RF exerts both the antioxidant and anti-inflammatory effects against AA-induced colonic inflammation by suppressing neutrophil accumulation, inhibiting reactive oxidant generation, preserving endogenous glutathione, improving oxidative DNA damage and regulating inflammatory mediators, suggesting a future potential role in the treatment and prevention of ulcerative colitis.