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    Effects of hyperthyroidism on expression of vascular endothelial growth factor (VEGF) and apoptosis in fetal adrenal glands
    (Pagepress Publ, 2015) Karaca, T.; Uz, Y. Hulya; Karabacak, R.; Karaboga, I.; Demirtas, S.; Cicek, A. Cagatay
    This study investigated the expression of vascular endothelial growth factor (VEGF), vascular density and apoptosis in fetal rat adrenal glands with hyperthyroidism in late gestation. Twelve mature female Wistar albino rats with the same biological and physiological features were used for this study. Rats were divided into two groups: control and hyperthyroidism. Hyperthyroidism was induced by daily subcutaneous injections of L-thyroxine (250 mu g/kg) before pregnancy for 21 days and during pregnancy Rats in the control and hyperthyroidism groups were caged according to the number of male rats. Zero day of pregnancy (Day 0) was indicated when the animals were observed to have microscopic sperm in vaginal smears. Pregnant rats were sacrificed on the 20th day of pregnancy; blood from each animal was collected to determine the concentrations of maternal adrenocorticotropic hormone and thyroxine. Rat fetuses were then quickly removed from the uterus, and the adrenal glands of the fetuses were dissected. VEGF expression, vascular density and apoptosis were analyzed in fetal rat adrenal glands. Maternal serum levels of the ACTH and free thyroxine were significantly higher in the hyperthyroidism group than in the control group. Immunohistochemistry revealed that the number of VEGF positive cells and vessel density significantly increased in the hyperthyroidism rat fetal adrenal group compared with the control group. Hyperthyroidism did not change the fetal and placental weights and the number of fetuses. This study demonstrates that hyperthyroidism may have an effect on the development of rat adrenal glands mediated by VEGF expression, angiogenesis, and apoptosis.
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    The efficacy of tyrosine kinase inhibitor dasatinib on colonic mucosal damage in murine model of colitis [Meeting Abstract]
    (Oxford Univ Press, 2016) Can, G.; Ayvaz, S.; Can, H.; Karaboga, I.; Demirtas, S.; Aksit, H.; Yilmaz, B.
    [Abstract Not Available]
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    Pendrin and sodium/iodide symporter protein expression in the testicular tissue of normal and diabetic rats in prepubertal and post pubertal stages
    (Shiraz Univ, 2018) Karaca, T.; Demirtas, S.; Goren, Uzun D.
    Pendrin (PDS) and sodium/iodide symporter (NIS) are transmembrane proteins that are located in numerous tissue types, particularly thyroid follicular epithelial cells, where they are entrusted with the regulation of iodine molecules. In the present study, we aimed to clarify changes in PDS and NIS protein expression, in the testicular tissue of prepubertal and post pubertal rats at normal or diabetic conditions. Forty Wistar albino male rats (20 prepubertal and 20 post pubertal) were divided into four groups, as follows: group I was prepubertal control, group II was prepubertal diabetic (60 mg/kg intraperitoneal [ip] streptozotocin [STZ]), group III was post pubertal control, and group IV was post pubertal diabetic (60 mg/kg ip STZ). Ki67 immunoreactivity decreased in testicular tissue of both the prepubertal and post pubertal diabetic groups; the apoptotic tubule index and apoptotic cell number increased in the diabetic groups as compared to the control groups. Pendrin immunoreactivity was detected in seminiferous tubules and Leydig cells; and was significantly reduced in the diabetic groups (P<0.05). The number of cells positive for NIS was significantly decreased in prepubertal and post pubertal rats with diabetes, compared to the controls. Enzyme-linked immunosorbent assay (ELISA) analysis showed that PDS and NIS values were significantly reduced in the prepubertal and post pubertal diabetic groups as compared to the control groups. Our results indicate a potential relationship between puberty and PDS and NIS expression in rat testicular tissue and showed the decreasing effects of diabetes on PDS and NIS expression in testicular tissues in rats.
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    Spleen tyrosine kinase (Syk) inhibitor fostamatinib limits tissue damage and fibrosis in a bleomycin-induced scleroderma mouse model
    (Clinical & Exper Rheumatology, 2015) Pamuk, O. N.; Can, G.; Ayvaz, S.; Karaca, T.; Pamuk, G. E.; Demirtas, S.; Tsokos, G. C.
    Objective. The pathogenesis of fibrosis in scleroderma (SSc) is unknown. TGF-beta and platelet-derived growth factor are important in the development of fibrosis and tyrosine kinases are involved in these pathways. The possible antifibrotic effects of various kinase inhibitors in SSc have been studied before. Spleen tyrosine kinase (Syk) is a protein tyrosine kinase which activates intracellular signal transduction pathways; and has been claimed to be involved in the pathogenesis of systemic autoimmune diseases. Inhibition of Syk suppresses IgE-and IgG-associated FcR signal activation in various cell types; and suppresses experimental arthritis and skin and kidney disease in lupus-prone mice. We investigated the ability of a small drug, the Syk inhibitor, fostamatinib, to protect mice from bleomycin-induced SSc. Methods. Four study groups of BALB/c mice were included into this study: control, bleomycin (administered subcutaneously to BALB/c mice for 21 days), bleomycin and fostamatinib (mice fed with chow containing a Syk inhibitor for 21 days), and fostamatinib alone groups. Skin and lung tissue specimens were obtained and evaluated histologically. Results. Treatment with fostamatinib significantly reduced skin thickness and fibrosis. Mice treated with fostamatinib also displayed less fibrosis and inflammation in the lung tissue. Following fostamatinib treatment, Syk, phospho-Syk, and TGF-beta expression decreased in both skin and lung tissues. Conclusion. The Syk inhibitor fostamatinib prevented bleomycin-induced fibrosis and inflammation in the skin and in the lung. The anti-fibrotic effect of fostamatinib is linked to reduced Syk phosphorylation and TGF-beta expression. The Syk pathway appears as a potential molecular target for therapeutic intervention in SSc.