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Yazar "Kanit, L." seçeneğine göre listele

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    Decreased anxiety-like behavior in a selectively bred high nicotine-preferring rat line
    (Taylor and Francis Ltd., 2023) Bayoglu, M.; Ozturk, Bintepe, M.; Kanit, L.; Balkan, B.; Gozen, O.; Koylu, E.O.; Keser, A.
    Genetic vulnerability contributes significantly to the individual variability observed in nicotine dependence. Selective breeding for sensitivity to a particular effect of abused drugs has produced rodent lines useful for studying genetic vulnerability to drug addiction. Previous research showed that anxiety-related personality traits are associated with nicotine dependence. Therefore, we examined the differences in anxiety-like behavior between a high nicotine-preferring rat line and their controls. At the beginning of the study, all rats, naïve to any drug, were exposed sequentially to open field arena, marble-burying and elevated plus-maze paradigms. In the second step, all rats received nicotine in drinking water for 7 weeks. Behavioral tests were rerun on the final 2 weeks of chronic nicotine treatment. Elevated plus-maze testings under basal condition and during chronic nicotine treatment showed that the time spent on the open arms, preference for being in the open arms, and the latency to enter the closed arms were higher, whereas open arm avoidance index was lower in nicotine-preferring rats compared to the controls. In the open field test, nicotine-preferring rats spent longer time in the central zone and excreted less fecal pellets; they buried less marbles in the marble-burying test. These findings indicate a lower level of anxiety-like behavior in nicotine-preferring rat line under basal conditions and during chronic nicotine treatment. We conclude that lower anxiety level in nicotine-preferring rat line is consistent with novelty-seeking personality type and may increase vulnerability to nicotine dependence in this rat line. © 2023 Informa UK Limited, trading as Taylor & Francis Group.
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    Immunohistochemical evaluation of cell proliferation and apoptosis markers in ovaries and uterus of tamoxifen-treated rats
    (Blackwell Publishing, 2008) Cirpan, T.; Terek, M. C.; Ulukus, M.; Ulukus, E. C.; Akman, L.; Kanit, L.
    The aim of the study was to evaluate the immunohistochemical expression of cell proliferation and apoptosis markers in the ovaries and uterus of tamoxifen-treated rats. Twelve rats (150-200 g) were divided into two equal groups. The study group received daily intraperitoneal injections of tamoxifen dissolved in 5% dimethyl sulfoxide (n = 6). The control group received only the vehicle (n = 6). The rats were sacrificed at the 20th day of injection and were perfused. The ovaries and uterus of the rats were extracted. The sections were immunohistochemically stained with cell proliferation marker Ki-67 and the apoptosis markers PTEN and CD95. The expressions of the markers were quantified by a semiquantitative H-score method in myometrium, endometrial glands, ovarian surface epithelium, ovarian follicles, corpus luteum, and ovarian stroma separately. The mean H-scores of CD95 and PTEN obtained from myometrium, glandular endometrium, ovarian surface epithelium, ovarian follicles, corpus luteum, and ovarian stroma did not show significant difference between the study and the control groups. Proliferative index (Ki-67) of endometrial glands was significantly higher in the study group than in the control group (P < 0.05). In addition, proliferative index (Ki-67) of corpus luteum was significantly higher in the study group than in the control group (P < 0.05). Tamoxifen treatment has a potential to stimulate the cell proliferation of endometrial glands and corpus luteum in tamoxifen-treated rats. Apoptosis markers of PTEN and CD95 did not demonstrate significant difference after the tamoxifen treatment.
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    In vitro effects of ritodrine, magnesium sulfate and their combination on spontaneous contractions of myometrial strips of pregnant rat uteri
    (I R O G Canada, Inc, 2007) Hacivelioglu, S.; Cirpan, T.; Terek, M. Cosan; Kanit, L.; Kazandi, M.; Oztekin, K.
    Objective: To investigate in vitro effects of ritodrine, magnesium sulfate and their combination on spontaneous contractions of myometrial strips obtained from pregnant rat uteri. Method: A total of 13 pregnant Sprague Dawley rats with weights between 180-200 g were used in this study. Three strips from each rat were kept in an organ bath containing 20 rut Krebs-Henseleit Solution (pH: 7.4 and 37 degrees C. 10(-8), 10(-6) and 10(-4) M concentrations of ritodrine, magnesium Sulfate and the combination was applied over myometrial strips in Groups I (n: 10), 11 (1): 10) and III (n: 8), respectively. Amplitude and frequency of spontaneous myometrial contractions, which were recorded at the beginning of each experiment, were considered as reference values. Amplitude and frequency changes in spontaneous myometrial contractions were calculated at approximately ten-minute intervals right after the application of drugs as the percentage of difference at the first reference response. Results: Magnesium sulfate application did not lead to any significant difference on the amplitude and frequency of contractions at any of its concentrations. 10(-6) and 10(-4) M concentrations of ritodrine caused a significant decrease in the amplitude of contractions. It was also found that ritodrine significantly decreased the frequency values at all concentrations. A significant decrease in amplitude was observed at 10(-6) and 10(-4) M concentrations in the combination group. No significant decrease in frequency values was found at any concentration in the combination group. Conclusion: The tocolytic effect of ritodrine is Superior to that of magnesium sulfate.
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    Nicotinamide treatment reduces the levels of oxidative stress, apoptosis, and PARP-1 activity in A beta (1-42)-induced rat model of Alzheimer's disease
    (Informa Healthcare, 2014) Bayrakdar, E. Turunc; Uyanikgil, Y.; Kanit, L.; Koylu, E.; Yalcin, A.
    The underlying mechanisms of Alzheimer's Disease (AD) are still unclear. It is suggested that poly(ADP-ribose) polymerase-1(PARP-1) overactivation can cause neuroinflammation and cell death. In this study we searched the effects of nicotinamide(NA), endogenous PARP-1 inhibitor, on oxidative stress, apoptosis, and the regulation of PARP-1 and nuclear factor kappa B(NF-kappa B) in amyloid beta peptide(1-42)(A beta(1-42))-induced neurodegeneration. Sprague-Dawley rats were divided into four groups as control, A beta(1-42), A beta(1-42) + NA(100 and 500 mg/kg). All groups were stereotaxically injected bilaterally into the hippocampus with A beta(1-42) or saline. After surgery NA administrations were made intraperitoneally(ip) for 7 days. In order to investigate the effects of A beta(1-42) and NA, protein carbonyls, lipid peroxidation, reactive oxygen species(ROS) production, glutathione(GSH) levels, activities of antioxidant enzymes(catalase, superoxide dismutase, glutathione peroxidase), mitochondrial function, mRNA and protein levels of PARP-1, NF-kappa B, p53, Bax, and Bcl-2 were measured in specific brain regions such as cortex and hippocampus. A beta(1-42) treatment only increased the oxidative stress parameters and caused decline in antioxidant enzyme activities, mitochondrial function, and GSH levels. Also, overexpression of PARP-1, NF-kappa B, p53, Bax, and the decreased levels of Bcl-2 were observed in A beta(1-42)-treated group. NA treatments against A beta(1-42)-upregulated Bcl-2 and downregulated PARP-1, NF-kappa B, p53, and Bax levels. NA treatments also decreased the oxidative stress parameters and elevated antioxidant enzyme activities, GSH levels, and mitochondrial function against A beta(1-42) treatment. These data suggest that NA may have a therapeutic potential in neurodegenerative processes due to the decreased levels of oxidative stress, apoptosis, and PARP-1 activity.

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