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    CENTRAL NERVOUS SYSTEM COMPLICATIONS OF DIABETES IN STREPTOZOTOCIN-INDUCED DIABETIC RATS: A HISTOPATHOLOGICAL AND IMMUNOHISTOCHEMICAL EXAMINATION
    (Taylor & Francis Ltd, 2009) Guven, Aysel; Yavuz, Ozlem; Cam, Meryem; Comunoglu, Cem; Servinc, Ozdemir
    Diabetes mellitus is a common, potentially serious metabolic disorder. Over the long term, diabetes leads to serious consequences in a number of tissues, especially those that are insulin insensitive (retina, neurons, kidneys). It also causes a variety of functional and structural disorders in the central and peripheral nervous systems. We investigated whether neurodegenerative changes were observable in the hippocampus, cortex, and cerebellum after 4 weeks of streptozotocin (STZ)-induced diabetes in rats and the effect(s) of melatonin. Male Wistar rats (n = 32) were divided into four groups (n = 8 each): untreated controls, melatonin-treated controls, untreated diabetics, and melatonin-treated diabetics. Experimental diabetes was induced by a single dose of STZ (60 mg/kg, intraperitoneal (ip)). For 3 days before the administration of STZ, melatonin (200 mu g/kg/day, ip) was injected and continued for 4 weeks. Sections of hippocampus, cortex, and cerebellum were stained with hematoxylin and eosin and examined using light microscopy. In addition, brain tissues were examined immunohistochemically for the expression of glial and neuronal markers, including glial fibrillary acidic protein (GFAP), neuron-specific enolase (NSE), and heat shock protein-70 (HSP-70). No neurodegenerative changes were observed in the hippocampus, cortex, or cerebellum of the untreated diabetic group after 4 weeks compared with the other groups. We did not observe any change in GFAP, NSE, or HSP-70 immunostaining in the brain tissues of STZ-induced diabetic rats. In summary, after 4 weeks of STZ-induced diabetes in rats, no degenerative or immunohistochemical changes were detected in the hippocampus, cortex, or cerebellum.
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    Experimental acute myocardial infarction in rats: HIF-1?, caspase-3, erythropoietin and erythropoietin receptor expression and the cardioprotective effects of two different erythropoietin doses
    (Elsevier Gmbh, Urban & Fischer Verlag, 2013) Bagla, Aysel Guven; Ercan, Ertugrul; Asgun, Halil Fatih; Ickin, Meltem; Ercan, Feriha; Yavuz, Ozlem; Bagla, Suat
    The cardioprotective effects of two different doses of erythropoietin administration were analyzed in rats with experimental myocardial infarction. None, saline, standard-dose (5000 U kg(-1)) and high-dose (10,000 U kg(-1)) of human recombinant erythropoietin alpha were administered intraperitoneally in Wistar rats with myocardial infarction induced by coronary artery ligation. Infarct sizes measured after triphenyltetrazolium chloride staining, levels of biochemical markers, histopathology examined by light and electron microscopy, and immunohistochemical expressions of erythropoietin, erythropoietin receptor, hypoxia inducible factor-1 alpha and caspase-3, were analyzed. Lower scores of infarction and hemorrhage, lower number of macrophages and higher score of vascularization surrounding the infarct area were observed in the erythropoietin administered groups (p < 0.05). Erythropoietin administration after myocardial infarction reduced the area of infarction and hemorrhage. There were hypoxia inducible factor-1 alpha and caspase-3 expressions in the marginal area, and erythropoietin and erythropoietin receptor expression in both marginal and normal areas (p < 0.001). Vascularization, erythropoietin expression in the normal area and vascular erythropoietin expression were positively correlated with human erythropoietin levels. The cardioprotective effects of erythropoietin treatment were independent of endogenous erythropoietin/erythropoietin receptor activity. Moreover exogenous erythropoietin treatment did not suppress endogenous erythropoietin. Erythropoietin administration after myocardial infarction reduced caspase 3 expression (apoptotic activity) and induced neovascularization around the infarct area. Higher erythropoietin administration did not provide an additional benefit over the standard-dose in myocardial protection. (C) 2013 Elsevier GmbH. All rights reserved.
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    Orexin and adiponectin in high fat diet-induced insulin resistance
    (Taylor & Francis Ltd, 2019) Gulen, Meltem Ickin; Bagla, Aysel Guven; Yavuz, Ozlem; Hismiogullari, Adnan Adil
    Orexin A (OXA) is a hypothalamic neuropeptide with both central and peripheral activities on insulin signaling and energy balance. Adiponectin is an adipocytokine which regulates metabolisms of lipid and glucose via its receptors AdipoR1 and AdipoR2. This study investigated immunohistochemical changes in expressions of OXA, its receptor OX1R in pancreas and AdipoR1 in skeletal muscle with a high fat diet (HFD)-induced insulin resistance (IR). Standard 45% fat and 60% fat diets were administered to Wistar rats for 3 and 8 w. OXA expression increased with both 3- and 8-w 45% fat diets. OX1R expression also increased with a 3-w 45% fat diet, but decreased with the 3-w 60% fat diet. OXA, OX1R, and AdipoR1 expressions decreased with a 8-w 60% fat diet. An early adaptation in context of OXA was observed in pancreas beta-cell to HFD-induced IR. OXA, OX1R, and AdipoR1 expressions decreased with either the higher amount or longer duration of HFD consumption.
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    Pyrrolidine dithiocarbamate attenuates the development of monocrotaline-induced pulmonary arterial hypertension
    (Elsevier Gmbh, Urban & Fischer Verlag, 2013) Yavuz, Taner; Uzun, Ozge; Macit, Asli; Comunoglu, Cem; Yavuz, Ozlem; Silan, Coskun; Yuksel, Hatice
    We aimed to demonstrate the potential protective effects of pyrrolidine dithiocarbamate (PDTC) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). Adult male rats were randomly assigned to 4 groups: control group, MCT-treated rats only, MCT-injected rats treated with PDTC, and PDTC-treated rats only. Blood and tissue samples were collected after the sacrifice. Levels of malondialdehyde (MDA) were measured by using the thiobarbituric acid method. Total antioxidant status (TAS) was determined using a commercially available ImAnOx kit. A histopathological evaluation was accomplished by scoring the degree of severity. Endothelial damage of the main pulmonary artery was evaluated by immunohistochemical labeling of endothelial cells using anti-rat endothelial cell antigen 1 (RECA-1) antibody. MCT-induced right ventricular hypertrophy (RVH) was reduced significantly in the MCT + PDTC-treated group. MDA levels were significantly lowered in the MCT + PDTC-treated group. TAS was significantly higher in the MCT + PDTC-treated group when compared with the rats with PAH. Histopathological examination demonstrated that PDTC treatment reduced the development of inflammation, hemorrhage and congestion, and collagen deposition. In conclusion, PDTC attenuated PAH and protected pulmonary endothelium in rats administered MCT. These findings suggest that PDTC treatment may provide a new effective therapeutic approach in the treatment of PAH. (C) 2013 Elsevier GmbH. All rights reserved.