Yazar "Duran, Y." seçeneğine göre listele

Listeleniyor 1 - 3 / 3
  • Küçük Resim
    Öğe
    Effect of hesperetin on systemic inflammation and hepatic injury after blunt chest trauma in rats
    (Taylor and Francis Ltd, 2020) Duran, Y.; Karaboğa, İhsan
    We investigated the protective effect of hesperetin on hepatic damage after blunt chest trauma in rats using histological and biochemical methods. We used 18 adult male rats in three groups of six: control, chest trauma and chest trauma + hesperetin. Chest trauma was caused by dropping a metal cylinder onto the right hemithorax. Hesperetin, 100 mg/kg, was administered orally for 7 days. At the end of the seventh day, liver tissue samples were obtained. Serum tumor necrosis factor-alpha (TNF-?), interleukin 1-beta (IL-1?), alanine aminotransferase (AST), aspartate transferase (ALT) and lactate dehydrogenase (LDH) enzyme activities were measured in blood samples taken from the heart. The general structure of liver tissue was investigated using hematoxylin and eosin staining. Nuclear factor kappa beta (Nf-??) expression in liver tissue was determined by the indirect immunohistochemical method. Apoptosis was determined using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) method. Decreased TNF-?, AST and ALT enzyme activity, fewer histopathological changes and lower Nf-kB expression were observed in the hesperetin treated group compared to the chest trauma group. We also found reduced hepatic apoptosis in the chest trauma + hesperetin group compared to the chest trauma group. Hesperetine inhibits liver damage by reducing proinflammatory cytokines and by suppressing Nf-?? activity in a blunt chest trauma model in rats. © 2019, © 2019 The Biological Stain Commission.
  • Küçük Resim
    Öğe
    Protective effects of hesperetin on lipopolysaccharide-induced acute lung injury in a rat model
    (Baycinar Medical Publishing, 2020) Kaya, S.; Kaya, S.A.; Polat, E.; Erboğa, Zeynep Fidanol; Duran, Y.; Polat, Fatin Rüştü; Karaboğa, İhsan
    Background: In this experimental study, we aimed to investigate the effects of hesperetin, a natural flavonoid, on a lipopolysaccharideinduced acute lung injury model in rats. Methods: Between March 2019 and May 2019, a total of 18 adult male Wistar albino rats, weighing approximately 250 to 300 g, were randomly divided into three groups as control, lipopolysaccharide, and lipopolysaccharide + hesperetin groups (n=6 in each group). The wet/dry weight ratio of lung tissue was determined. Histopathological changes were examined using light and scanning electron microscopy. Pulmonary nuclear factor-kappa beta, inducible nitric oxide synthase, and alpha-smooth muscle antigen activity were determined with indirect immunohistochemical methods. Pulmonary apoptosis was detected with the terminal deoxynucleotidyl transferase dUTP nick-end labeling method. Tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, and interleukin-10 concentrations were measured with enzyme-linked immunosorbent assay. Results: Treatment with hesperetin significantly improved the architecture of lung tissue and reduced the wet/dry weight ratio, nuclear factor-kappa beta, inducible nitric oxide synthase, and alphasmooth muscle antigen expression, pulmonary apoptosis, and levels of proinflammatory cytokines. Conclusion: Our study results suggest that hesperetin has a potent protective effect against lipopolysaccharide-induced acute lung injury in rats via suppression of the proinflammatory cytokine cascade, nuclear factor-kappa beta, signaling pathway activation, and apoptosis. © 2020 All right reserved by the Turkish Society of Cardiovascular Surgery.
  • Küçük Resim
    Öğe
    Royal jelly attenuates gastric mucosal injury in a rat ethanol-induced gastric injury model
    (Springer Science and Business Media B.V., 2020) Duran, Y.; Karaboğa, İhsan; Polat, Fatin Rüştü; Polat, E.; Erboğa, Zeynep Fidanol; Ovalı, M. A.; Yılmaz, A.; Çelikkol, A.
    The aim of the study was to investigate traditionally used Royal Jelly (RJ) for treating an ethanol-induced gastric ulcer model in rats. A total of 32 Wistar albino male rats were divided into 4 groups of 8: group I = Control, group II = Ethanol, group III = RJ + Ethanol, and group IV = Lansoprazole + Ethanol. In groups II, III, and IV, animals were administered 1 ml of absolute ethanol orally after a 24-h fast to induce ulcer formation. The histopathological changes in the gastric mucosa were determined using hematoxylin-eosin (H&E) staining. Immunohistochemically, inducible nitric oxide (iNOS) and nuclear factor kappa beta (Nf-??) markings were evaluated in gastric tissue. Cell death in the gastric mucosa was determined by the TUNEL method. Oxidative status markers, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), and myeloperoxidase (MPO) levels were determined spectrophotometrically. Expression of the interleukin – 1 beta (IL-1?) and tumor necrosis factor-? (TNF-?) genes in gastric tissues was determined by real-time PCR; and TNF-?, IL-10, and IL-1? levels were determined. RJ was found to inhibit iNOS and Nf-?? activity in the gastric mucosa and prevent epithelial cell apoptosis. In particular, pro-inflammatory cytokines TNF-? and IL-1? levels were significantly decreased in the RJ + Ethanol group compared to the Ethanol group. In addition, a decrease in the MPO level indicated that RJ prevented tissue damage, especially by preventing inflammatory cell infiltration. The study demonstrated a possible gastroprotective effect of RJ in a rat ethanol-induced gastric ulcer model. © 2020, Springer Nature B.V.