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    Brain abscess and bronchopneumonia caused by acinetobacter baumannii in a 2-year-old femalesheep
    (Taylor & francıs ltd, 2-4 park square, mılton park, abıngdon or14 4rn, oxon, england, 2018) Eroksuz, Yesari; Otlu, Baris; Eroksuz, Hatice; Gursoy, Nafia Canan; Yerlikaya, Zeynep; Incili, Canan Akdeniz; Karabulut, Burak; Timurkaan, Necati; Timurkan, Mehmet Ozkan
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    The effects of hesperidin on idiopathic pulmonary fibrosis evaluated by histopathologial-biochemical and micro-computed tomography examinations in a bleomycin-rat model.
    (Allied Acad, 2016) Gormeli, Cemile Ayse; Sarac, Kaya; Ciftci, Osman; Timurkaan, Necati; Malkoc, Siddik
    Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive parenchymal lung disease. The pathology is characterized by recurrent injury to microscopic alveolar epithelial cells. These injuries activate inflammatory cells, resulting in the proliferation of fibroblasts and alveolar tissue damage. Interstitial inflammation, advanced oxidative stress, and abnormal antioxidant activity were demonstrated to be the main causes of IPF. Hesperidin (HP) is a bioflavonoid with anti-inflammatory, antioxidant, anticarcinogenic, and analgesic actions. HP may be able to prevent pulmonary fibrosis, and may ultimately lead to healthy lung function. We hypothesized that HP could prevent Bleomycin (BLC)-induced pulmonary fibrosis due to its biochemical, antioxidant, and anti-inflammatory properties and may ultimately lead to healthy lung function. Based on these findings, we hypothesized that HP could prevent BLC-induced pulmonary fibrosis due to its biochemical, antioxidant, and anti-inflammatory properties. The animals were divided into 4 groups with 14 rats per group. The experimental treatments were as follows: Control, BLC, HP, and BLC+HP. Six of the 14 lungs in each group were sent for micro CT analysis. The remaining 8 lung specimens were harvested for histopathological and biochemical analyses. BLC-treated rats showed marked histopathological changes in the lungs. In these rats, thickening of interalveolar septa due to macrophage and lymphocyte infiltration, as well as fibroblast proliferation, were observed. Histopathological changes were less severe in the BLC+HP group compared with the BLC group. HP treatment led to a decrease in lipid peroxidation and an increase in antioxidant status compared with the BLC group. Also micro-CT showed a significant positive correlation with histopathological and biochemical results. To the best of our knowledge, this is the first study to evaluate the beneficial effects of HP against pulmonary fibrosis using histopathological, biochemical, and micro-CT analyses and HP successfully minimized the severity of BLC-induced lung injury, which was used as a model for IPF.
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    Protective effects of protocatechuic acid on TCDD-induced oxidative and histopathological damage in the heart tissue of rats
    (Sage Publications Inc, 2013) Ciftci, Osman; Disli, Olcay Murat; Timurkaan, Necati
    2,3,7,8-Tetracholorodibenzo-p-dioxin (TCDD) is a highly toxic environmental contaminant that causes severe toxic effects in animal and human. In this study, we investigated the toxic effects of TCDD and the preventive effects of protocatechuic acid (PCA), a widespread phenolic compound, in the heart tissue of rats. For this purpose, 3-4 months old 28 rats with 280-310g body weights were equally divided into 4 groups (control, TCDD, PCA, TCDD+PCA group). A 2g/kg dose of 2,3,7,8-TCDD and 100mg/kg dose of PCA were dissolved in corn oil and given orally to the rats for 45 days. The results indicated that TCDD induced oxidative stress by increasing the level of thiobarbituric acid reactive substance and by decreasing the levels of glutathione, catalase, glutathione peroxidase and superoxide dismutase in the heart tissue of rats. In contrast, PCA treatment prevents the toxic effects of TCDD on oxidative stress. In addition, histopathological alterations such as necrosis and hemorrhage occurred in TCDD group, and PCA treatment partially prevents these alterations in heart tissue. In this study, it was concluded that TCDD exposure led to toxic effects in heart tissue and PCA treatment could prevent the toxicity of TCDD.