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    Investigation of the effects of naringin on intestinal ischemia reperfusion model at the ultrastructural and biochemical level
    (Elsevier France-Editions Scientifiques Medicales Elsevier, 2019) Bakar, E.; Ulucam, E.; Cerkezkayabekir, A.; Sanal, F.; Inan, M.
    We aimed to evaluate the ultrastructural effect of reversing cellular damage, occurring in rats due to ischemia-reperfusion (I/R) in the intestine, with naringin implementation through biochemical parameters. Rats were divided the sham/control, I/R and the naringin groups (n=7). For I/R group, 120 min of ischemia and 120 min of reperfusion was applied to the superior mesenteric artery. In the naringin group, after 120 min, 50 mg/kg naringin was implemented, and then 120 min of reperfusion was applied. Morphological evaluation was performed via Chiu score and electron microscopy. The antioxidant parameters were examined. Chiu score in I/R (p < 0.01) and naringin (p < 0.05) groups were higher than the sham/control group. In ultrastructural level some irregularity were observed in I/R group. Although it decreased in the naringin group, the damage was observed to continue. Malondialdehyde (MDA) amount and Superoxide dismutase activity (SOD) in I/R group were higher in comparison to the sham/control group (p < 0.01), while glutathione peroxidase activity (Gpx) was found to be lower (p < 0.01). SOD (p < 0.05) and MDA (p < 0.01) were decreased by naringin group. Gpx was decreased in I/R group compared to sham/control group (p < 0.01) and elevated due to naringin administration (p < 0.05). Catalase activity was observed to decrease in the naringin group compared to control and I/R groups (p < 0.01). It was determined that naringin provided limited healing at the ultrastructural level but also effected recovery within antioxidant parameters.
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    Mesenchymal stem cells increase antioxidant capacity in intestinal ischemia/reperfusion damage
    (W B Saunders Co-Elsevier Inc, 2017) Inan, M.; Bakar, E.; Cerkezkayabekir, A.; Sanal, F.; Ulucam, E.; Subasi, C.; Karaoz, E.
    Background: Mesenchymal stemcells (MSCs) may have beneficial effects in reversing intestinal damage resulting fromcirculatory disorders. The hypothesis of this study is thatMSCs increase antioxidant capacity of small bowel tissue following intestinal ischemia reperfusion (I/R) damage. Methods: A total of 100 rats were used for the control group and three experimental groups, as follows: the sham control, local MSC, and systemic MSC groups. Each group consisted of 10 animals on days 1, 4, and 7 of the experiment. Ischemiawas established by clamping the superior mesenteric artery (SMA) for 45min; following this, reperfusion was carried out for 1, 4, and 7 days in all groups. In the local and systemic groups, MSCs were administered intravenously and locally just after the ischemia, and they were investigated after 1, 4, and 7 days. The superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (Gpx) activities, as well as malondialdehyde (MDA) and total protein levels, were measured. Histopathological analysis was performed using light and electron microscopy. The indicators of proliferation from the effects of anti-and pro-inflammatory cytokines were evaluated using immunohistochemistry. Results: MDA was increased (P < 0.05) in the sham control group and decreased (P < 0.05) in the MSC groups. SOD, CAT, and Gpx were decreased in the localMSC group (P < 0.05). The highest level of amelioration was observed on day 7 in the local MSC group via light and electron microscopy. It was found that the MSCs arrived at the damaged intestinal wall in the MSC groups immediately after injection. Pro-inflammatory cytokines interleukin-1 beta(IL1 beta), transforming growth factor-beta 1 (TGF beta 1), tumor necrosis factor-alpha (TNF alpha), IL6, MIP2, and MPO decreased (P < 0.05), while anti-inflammatory cytokines EP3 and IL1ra increased (p < 0.05) in the local and systemic MSC groups. In addition, proliferation indicators, such as PCNA and KI67, increased (P < 0.05) in the local and systemic MSC groups. Conclusions: Parallel to our hypothesis, MSC increases the antioxidant capacity of small bowel tissue after intestinal I/R damage. The MSCs migrated to the reperfused small intestine by homing and reduced oxidative stress via the effects of SOD, CAT, and Gpx, as well as reducing the MDA level; thus, they could increase antioxidant capacity of intestine and have a therapeutic effect on the damaged tissue. We think that this effectwas achieved via scavenging of oxygen radicals, suppression of pro-inflammatory cytokines, and increasing the expression of anti-inflammatory cytokines. (C) 2017 Elsevier Inc. All rights reserved.
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    Naringin protects viscera from ischemia/reperfusion injury by regulating the nitric oxide level in a rat model
    (Taylor & Francis Ltd, 2017) Cerkezkayabekir, A.; Sanal, F.; Bakar, E.; Ulucam, E.; Inan, M.
    We investigated the effects of naringin on small intestine, liver, kidney and lung recovery after ischemia/reperfusion (I/R) injury of the gut. Rats were divided randomly into four groups of eight. Group A was the sham control; group B was ischemic for 2 h; group C was ischemic for 2 h and re-perfused for 2 h (I/R); group D was treated with 50 mg/kg naringin after ischemia, then re-perfused for 2 h. Endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) expressions were detected by immunolabeling. We also measured arginase activity, amounts of nitric oxide (NO) and total protein. iNOS was increased significantly in the small intestine, liver and kidney in group C. iNOS was decreased significantly only in small intestine and lung in group D. eNOS was increased significantly in the small intestine, liver and lung in group C. eNOS was decreased in small intestine, liver and lung in group D; however, eNOS was decreased in the kidney in group C and increased in the kidney in group D. The amount of NO was decreased significantly in all tissues in group D, but arginase activity was decreased in the small intestine and lung, increased in the kidney and remained unchanged in the liver in group D. The total protein increased in the small intestine and liver in group D, but decreased significantly in the kidney and lung in group D. Naringin had significant, salutary effects on the biochemical parameters of I/R by decreasing the NO level, equilibrating iNOS and eNOS expressions, and decreasing arginase activity.
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    Protective effects of proanthocyanidin and vitamin E against toxic effects of formaldehyde in kidney tissue
    (Taylor & Francis Ltd, 2015) Bakar, E.; Ulucam, E.; Cerkezkayabekir, A.
    We investigated possible effects of proanthocyanidin (PA) and vitamin E on damage to rat kidneys induced by formaldehyde (FA), using biochemical characteristics and light and electron microscopy. Male rats were divided into control, FA, PA and vitamin E treated groups. Kidney tissue was observed by light and electron microscopy. Bcl-2/Bax rate was measured using immunohistochemistry. Malondialdehyde (MDA) and total sialic acid (TSA) levels, superoxide dismutase (SOD), glutathione peroxidase (Gpx), catalase (CAT) and myeloperoxidase (MPO) activities were measured. We found that FA caused damage to the parietal epithelial layer of the glomerulus, mononuclear cell infiltration, membrane damage in renal tubules, pyknotic nuclei, hypertrophic cells in Henle's loop and tubules, and loss of renal tubule integrity. We also observed invagination of the nuclear membrane, irregularity of chromatin material and loss of mitochondrial cristae. We observed increased Bcl-2 and Bax immunostaining in the FA group, but the Bcl-2/Bax rate remained unchanged in FA, PA and vitamin E groups compared to controls. Tissue MDA and TSA levels, and CAT and Gpx activities were increased, and SOD and MPO activities were decreased by FA toxicity. We observed a protective effect of PA in tissue MDA and TSA levels and SOD activities, because there was no difference in the PA group compared to the control group. We investigated the antioxidant effects of PA and vitamin E and found protective effects of PA against apoptosis.