Yazar "Ayvaz, S." seçeneğine göre listele
Listeleniyor 1 - 3 / 3
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe Effects of methylene blue in acute lung injury induced by blunt chest trauma(Lithographia, 2014) Ayvaz, S.; Aksu, B.; Karaca, T.; Cemek, M.; Tarladacalisir, Y-T; Ayaz, A.; Metin, M-SBackground: We studied whether methylene blue (MB) treatment blunts chest trauma-induced lung injury in rats. Material and Methods: Forty male Sprague-Dawley rats, 200-300g, were used. The rats were divided into five groups (n=8): control, early contusion (EC), early contusion + methylene blue (2 mg/kg, EC+MB), late contusion (LC), and late contusion + methylene blue (2 mg/kg, LC+MB). Results: Histopathological analysis showed increased hemorrhage, alveolar wall thickness, edema, and inflammatory cell infiltrates in the EC and LC rats, which decreased upon MB treatment. Immunohistochemical studies revealed that MB reduced activation of inducible nitric oxide synthase (iNOS) and the number of active terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells. A significant increase was observed in the malondialdehyde (MDA) and nitric oxide (NO) levels in the EC group compared to the control group (p<0.05). In addition, a significant decrease was reported in the glutathione (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels (p<0.01), but no significant difference was observed in the catalase (CAT) levels among the groups. The MDA level was significantly higher in the LC group compared to the control group, whereas the GSH level was significantly lower compared to the control group. The NO level in the EC+MB group was significantly lower when compared to the NO level in the EC group (p<0.05). Conclusion: The present study provides evidence that MB might serve as a therapeutic treatment for blunt chest trauma.Öğe 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]Öğe 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.