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    Effect of fullerenol C60 on lung and renal tissue in lower extremity ischemia-reperfusion injury in sevoflurane-treated rats
    (Spandidos Publ Ltd, 2024) Arpaci, Ayse Hande; Koksal, Zeynep; Yigman, Zeynep; Kucuk, Aysegul; Sivgin, Volkan; Arslan, Mustafa; Kavutcu, Mustafa; Akarca Dizakar, Saadet Özen
    The aim of the present study was to examine the effect of fullerenol C60 on lung and kidney tissue in sevoflurane-treated rats with lower extremity ischemia-reperfusion (IR) injury. A total of 30 Wistar albino rats weighing 225-275 g were used and were equally divided into five groups (n=6/group): i) Sham; ii) IR; iii) IR-fullerenol C60 (IR-FUL); iv) IR-sevoflurane; and v) IR-fullerenol C60-sevoflurane (IR-FUL-SEVO). Fullerenol C60 was administered intraperitoneally prior to lower extremity IR induction and sevoflurane was administered during the IR injury. Subsequently, lung and kidney histopathological examinations, and serum biochemical analyses were performed. Lung tissue showed markedly increased congestion and neutrophil infiltration in the IR group compared with in the sham group, and notable decreases in congestion and neutrophil infiltration were observed in the treatment groups compared with in the IR group. In the histopathological evaluation of the kidney samples, vacuolization, loss of brush border in tubular epithelial cells, tubular epithelial loss and varying degrees of tubular damage were observed in all groups that underwent IR. There was a significant increase in the mean renal tubule injury score in all IR groups compared with that in the sham group. In addition, the mean kidney injury score was significantly lower in the IR-FUL and IR-FUL-SEVO groups than that in the IR group. It was observed that the expression levels of tumor necrosis factor-alpha, interleukin 1 beta and intercellular adhesion molecule 1 in the lung and kidney tissues were increased following IR, and were decreased in the groups treated with fullerenol C60 and sevoflurane. Notably, it was determined that the reduction in cytokine expression was greatest in the IR-FUL group. When the oxidant status parameters in the lungs and kidneys were examined, thiobarbituric acid reactive substances levels, and catalase and glutathione S-transferase enzyme activities were significantly different in the groups receiving sevoflurane or fullerenol C60 treatment compared with those in the IR group. The present study demonstrated the protective effects of fullerenol C60 on the lung and kidney tissues of rats under sevoflurane anesthesia after establishment of lower extremity IR. The results of the present study showed that fullerenol C60 can reduce oxidative and histopathological damage in the lungs and kidneys following IR of the lower extremities.
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    Transauricular vagal nerve stimulation suppresses inflammatory responses in the gut and brain in an inflammatory bowel disease model
    (Wiley, 2024) Atalar, Kerem; Alim, Ece; Yigman, Zeynep; Belen, Hayrunnisa Bolay; Erten, Fusun; Sahin, Kazim; Soylu, Ayse; Dizakar, Saadet Özen Akarca
    Inflammatory bowel disease (IBD) encompasses Crohn's disease (CD) and ulcerative colitis (UC), is a major health problem on a global scale and its treatment is unsatisfactory. We aimed to investigate the effects of transauricular vagal nerve stimulation (tVNS) on inflammation in rats with IBD induced by trinitrobenzene sulfonic acid (TNBS). A total of 36 adult female Sprague-Dawley rats were given TNBS, or vehicle, and tVNS, or sham, every other day for 30 min for 10 days. Postmortem macroscopic and microscopic colon morphology were evaluated by histological staining. Additionally, IL-1 beta, IL-6, IL-10, and TNF-alpha cytokine levels in the colon and the brain were evaluated by immunohistochemistry and western blotting analysis. TNBS induced epithelial damage, inflammation, ulceration, and thickened mucosal layer in the colonic tissues. Administration of tVNS significantly ameliorated the severity of TNBS-induced tissue damage and inflammatory response. TNBS also alters pro-inflammatory and anti-inflammatory balance in the brain tissue. TVNS application significantly suppressed the protein levels of pro-inflammatory cytokines, namely IL-1 beta, IL-6, and TNF- alpha while augmenting the level of anti-inflammatory cytokine IL-10 in the colonic and the brain tissue. We have shown that TNBS-mediated colonic inflammation and tissue damage are associated with neuroinflammatory responses in the brain tissue. Also demonstrated for the first time that neuroinflammatory response in the gut-brain axis is suppressed by tVNS in the IBD model. Non-invasive tVNS stands out as a new potential treatment option for types of IBD.