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- MakaleAçık Erişim2016Scopus SJRQ2Increased expressions of eNOS and iNOS correlate with apoptosis of diabetic nephropathy in streptozotocin-induced type 1 diabetic rats; [Streptozotosin kaynaklı tip 1 diyabetik sıçanlarda meydana gelen nefropatilerde artan eNOS ve iNOS sunumlarının apoptozisle ilişkilendirilmesi]
Dinçel, Güngör Çağdaş; Yildirim, Serkan
The present study was designed to evaluate the effects of high level of nitric oxide (NO) production and oxidative stress (OS) on nephropathology and to identify whether NO and OS have any correlation with apoptosis seen in diabetic kidney, elucidating the underlying mechanism(s) involved in the development of nephropathology in streptozotocin (STZ)-induced diabetic rats. Expression levels of caspase 3, caspase 9, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), 8-hydroxy-2′-deoxyguanosine (8-OHdG), for the detection of oxidative damage to DNA, were examined in diabetic kidney tissues. Results of the study revealed that the levels of 8-OHdG (P<0.005), eNOS (P<0.005), iNOS (P<0.005), caspase 3 (P<0.005) and caspase 9 (P<0.005) were remarkably higher in diabetic kidney tissues than in controls. In addition, STZ-treated animals showed significant loss of body weight and renal enlargement. It was suggested that apoptosis, OS and increased NO levels are involved in the pathogenesis of diabetic nephropathy. The results also strongly suggested that STZ-induced apoptosis through activation of the intrinsic pathway and that might be most likely related to increased NO levels. Moreover, high NO production was not only mediated by eNOS but also by iNOS. Increased NO production may contribute to hyperfiltration and microalbuminuria in early diabetic nephropathy. Furthermore, expression of 8-OHdG might give an idea of the progress and may be essential as it has a diagnostic significance for this disease. In conclusion, we believe that eNOS and iNOS overexpressions induce diabetic nephropathy by mediating apoptosis in STZ-induced rats.
AtıfScopus4WoS4İncele - MakaleYalnız künye2015Scopus SJRQ2Nitric oxide production increases during Toxoplasma gondii encephalitis in mice
Dincel, Gungor Cagdas; Atmaca, Hasan Tarik
Toxoplasma gondii is an intracellular parasite with the potential of causing severe encephalitis among immunocompromised human and animals. The aim of this experimental study was to investigate the immunomodulatory and immunopathological role of nitric oxide (NO) in central nervous systems and to identify any correlation between toxoplasmosis neuropathology and investigate the consequences of the cellular responses protect against T. gondii. Mice were infected with ME49 strain T. gondii and levels of endothelial, neuronal and inducible nitric oxide synthase (eNOS, nNOS, iNOS), glial fibrillary acidic protein (GFAP) and neurofilament (NF) were examined in brain tissues by immunohistochemistry, during the development and establishment of a chronic infection at 10 30 and 60 days post infection. Results of the study revealed that the levels of eNOS (. p<0.05), nNOS (. p<0.05), iNOS (. p<0.005), GFAP (. p<0.005) and NF (. p<0.005) were remarkably higher in T. gondii-infected mice than in uninfected control. The most prominent finding from our study was 10 and 30 days after inoculation data indicating that increased levels of NO not only a potential neuroprotective role for immunoregulatory and immunopathological but also might be a molecular trigger of bradyzoite development. Furthermore, this findings were shown that high expressed NO origin was not only inducible nitric oxide synthase but also endothelial and neuronal. We demonstrated that activation of astrocytes and microglia/macrophages is a significant event in toxoplasma encephalitis (TE). The results also clearly indicated that increased levels of NO might contribute to neuropathology related with TE. Furthermore, expression of NF might gives an idea of the progress and critical for diagnostic significance of this disease.
AtıfScopus49WoS44OpenAlex53İncele