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    Effect of homocysteine on nitric oxide production in coronary microvascular endothelial cells
    (Taylor & Francis Inc, 2007) Erol, Ayse; Cinar, Mehtap G.; Can, Cenk; Murat, Olukman; Uelker, Sibel; Kosay, Sezen
    Hyperhomocysteinemia is widely recognized as an independent risk factor for coronary artery vascular disease, although the underlying mechanisms are not well understood. This study aims to investigate the effect of homocysteine on nitric oxide ( NO) production in coronary microvascular endothelial cells (CMECs) and putative mechanisms mediating this effect. CMECs were isolated on Langendorff system by collagenase perfusion of hearts from male rats and cultured. The effect of homocysteine (0.01 to 1 mM) on basal and stimulated NO production was evaluated by measuring nitrite in the culture media after incubation with or without N-G-nitro-L-arginine methyl ester (L-NAME) ( 1 mM), superoxide dismutase (100 U/mL), or catalase ( 1000 U/mL) for 24 h. Total nitrite was measured using Griess reaction after reduction of nitrate to nitrite with nitrate reductase. Homocysteine did not affect basal nitrite accumulation; however, it significantly increased the nitrite accumulation induced by the calcium ionophore A23187 or interleukin-1 beta only at 1 mM. This effect of homocysteine was significantly inhibited by L-NAME, superoxide dismutase, and catalase. In conclusion, homocysteine increases NO release from stimulated CMECs without affecting basal NO production, which is probably accompanied by increased production of reactive oxygen species. It can be postulated that endothelial cells generate NO in order to minimize the damage caused by homocysteine.
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    Neuroprotective effects of melatonin upon the offspring cerebellar cortex in the rat model of BCNU-induced cortical dysplasia
    (Elsevier Science Bv, 2007) Uyanikgil, Yigit; Baka, Meral; Ates, Utku; Turgut, Mehmet; Yavasoglu, Altug; Uelker, Sibel; Soezmen, Eser Yildirim; Sezer, Ebru; Elmas, Cigdem; Yurtseven, Mine Ertem
    Cortical dysplasia is a malformation characterized by defects in proliferation, migration and maturation. This study was designed to evaluate the alterations in offspring rat cerebellum induced by maternal exposure to carmustine-[1,3-bis (2-chloroethyl)-1-nitrosoure] (BCNU) and to investigate the effects of exogenous melatonin upon cerebellar BCNU-induced cortical dysplasia, using histological and biochemical analyses. Pregnant Wistar rats were assigned to five groups: intact-control, saline-control, melatonin-treated, BCNU-exposed and BCNU-exposed plus melatonin. Rats were exposed to BCNU on embryonic day 15 and melatonin was given until delivery. Immuno/histochemistry and electron microscopy were carried out on the offspring cerebellum, and levels of malondialdehyde and superoxide dismutase were determined. Histopathologic ally, typical findings were observed in the cerebella from the control groups, but the findings consistent with early embryonic development were noted in BCNU-exposed cortical dysplasia group. There was a marked increase in the number of TUNEL positive cells and nestin positive cells in BCNU-exposed group, but a decreased immunoreactivity to glial fibrillary acidic protein, synaptophysin and transforming growth factor beta 1 was observed, indicating a delayed maturation, and melatonin significantly reversed these changes. Malondialdehyde level in BCNU-exposed group was higher than those in control groups and melatonin decreased malondialdehyde levels in BCNU group (P<0.01), while there were no significant differences in the superoxide dismutase levels between these groups. These data suggest that exposure of animals to BCNU during pregnancy leads to delayed maturation of offspring cerebellum and melatonin protects the cerebellum against the effects of BCNU. (C) 2007 Elsevier B.V. All rights reserved.
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    Therapeutic concentrations of tacrolimus do not interfere with endothelial nitric oxide synthesis in rat thoracic aortas and coronary arteries
    (Lippincott Williams & Wilkins, 2007) Can, Cenk; Erol, Ayse; Cinar, Mehtap; Olukman, Murat; Uelker, Sibel; Evinc, Akguen
    This study aimed to investigate the potential effect of in vivo administration of immunosuppressive agent FK-506 (tacrolimus) on the endothelial function of rat thoracic aortas with respect to nitric oxide (NO) synthesis. In vitro effect of the drug on NO synthesis in cultured rat coronary microvascular endothelial cells (CMEC) was also studied. In vivo administration of tacrolimus (1 mg/kg/d, intramuscular) to rats for 14 days resulted in decreased relaxant responses to the higher concentrations (1 to 30 mu M) of acetylcholine in the aortas; however, responses to calcium ionophore A23187, sodium nitroprusside, L-arginine, and L-NAME did not change significantly. No changes were observed in phenylephrine-induced contractions in endothelium-denuded or -intact preparations. Administration of the vehicle for 14 days did not affect these parameters. In order to evaluate the in vitro effect of tacrolimus on NO release, CMEC isolated from rat hearts were incubated with either tacrolimus (0.01, 0.1 mu M) or the vehicle. Basal, calcium ionophore-stimulated, or interleukin-IP-induced NO synthesis was determined by measuring total nitrite in the media. Neither tacrolimus nor the vehicle changed nitrite accumulation. It has been concluded that therapeutic concentrations of tacrolimus do not alter NO production in rat thoracic aorta or cultured CMEC however, it impairs relaxant responses of rat aorta induced by higher concentrations of acetylcholine, possibly through changes in the downstream of receptor activation or through an imbalance between endothelium-dependent relaxant and contracting factors within the endothelium in favor of the contracting factor(s).