Sürdürülebilir Kalkınma Amaçları

• 7

• MakaleYalnız künye2016Scopus SJRQ3/r/gumushane/18830
  Streptozotosin Kaynaklı Tip 1 Diyabetik Sıçanlarda Meydana Gelen Nefropatilerde Artan eNOS ve iNOS Sunumlarının Apoptozisle İlişkilendirilmesi

  Dincel, Gungor Cagdas; 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.

  AtıfTR Dizin1

  İncele
• MakaleYalnız künye2016Scopus SJRQ2/r/gumushane/15330
  Increased expressions of ADAMTS-13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice

  Dincel, Gungor Cagdas; Atmaca, Hasan Tarik

  Toxoplasma gondii (T. gondii) is a protozoan parasite with the potential of causing severe encephalitis among immunocompromised humans and animals. Our previous study showed that T. gondii induces high nitric oxide (NO) production, high glial activation (GFAP) and neurofilament expressions, leading to severe neurodegeneration in toxoplasma encephalitis (TE) in the central nervous system (CNS). The aim of this experimental study was to investigate ADAMTS-13 expression and apoptosis in CNS and to identify whether they have any correlation with toxoplasmosis neuropathology and neurodegeneration. Mice were infected with ME49 strain T. gondii and the levels of ADAMTS-13, caspase 3, caspase 8, caspase 9, TNFR1 and Bcl-xL expressions were examined in brain tissues by immunohistochemistry, during the development and establishment of chronic infections at 10, 30 and 60days post-infection. Results of the study revealed that the levels of ADAMTS-13 (P < 0.005), caspase 3 (P < 0.05), caspase 8 (P < 0.05), caspase 9 (P < 0.005) and TNFR1 (P < 0.05) expressions in the brain markedly increased while Bcl-xL expression decreased (P < 0.005). The most prominent finding from our study was that 10, 30 and 60days post-infection ADAMTS-13 increased significantly and this may play an important role in the regulation and protection of the blood-brain barrier integrity and CNS microenvironment in TE. These results also suggest that T. gondii-mediated apoptosis might play a pivotal role and a different type of role in the mechanism of neurodegeneration and neuropathology in the process of TE. Furthermore, expression of ADAMTS-13 might give an idea of the progress and is critical for diagnosis of this disease. To the best of the authors' knowledge, this is the first report on ADAMTS-13 expression in the CNS of T. gondii-infected mice.

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  AtıfScopus31·WoS29·OpenAlex32

  İncele
• MakaleAçık Erişim2016Scopus SJRQ1/r/gumushane/15131
  Effect of piracetam and nimodipine on full-thickness skin burns in rabbits

  Sari, Elif; Dincel, Gungor C.

  The potential of several drugs for full-thickness skin burns has been investigated, but the treatment of such burns remains a challenge in plastic surgery. The present study was designed to determine the effect of systemic and topical administration of piracetam and nimodipine on full-thickness skin burn wound healing. A total of 36 New Zealand male rabbits were divided into six groups. Full-thickness skin burns were produced in all the groups, except the control group. Piracetam was administered systemically (piracetam-IV) and topically (piracetam-C) for 14 days, and nimodipine was administered systemically (nimodipine-IV) and topically (nimodipine-C) over the burn wounds for 14 days. The sham group underwent burn injury but was not administered any drug. After 21 days, gross examination and histopathological analysis were performed and the results were compared statistically. Nimodipine-C and nimodipine-IV had no effect on burn wound healing. However, both piracetam-IV and piracetam-C significantly enhanced the healing of the full-thickness skin burn wounds, although the latter was more effective, useful and practical in burn wound healing. The histopathological features of the wounds in the piracetam-C group were closer to those of the control group than those of the other groups. Piracetam-C rather than piracetam-IV may promote full-thickness burn wound healing in rabbits.

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  AtıfScopus2·WoS2·OpenAlex2

  İncele
• MakaleYalnız künye2016/r/gumushane/12969
  First detection of hypomyelination associated with bovine viral diarrhoea virus in an aborted calf in gumushane region

  Dinçel, Güngör Çaǧdaş; Gökhan, Nezihe

  In this study, hydranencephaly and mild cerebellar hypoplasia were reported macroscopically, microscopically and immunohistochemically in an aborted Holstein Friesian calf. A relationship between Bovine Viral Diarrhoea Virus (BVDV) infection and histopathology associated with the central nervous system (CNS) lesions were demonstrated. In the histopathology, perivascular haemorrhage, oedema, neuronal necrosis and degeneration were observed in the CNS. BVDV positive immunoreaction was detected in neurons, glial and endothelial cells of CNS by immunohistochemical examination. As far as the authors are concerned, this is the first report of BVDV present in an aborted Holstein Friesian Calf in Gumushane region. This finding may have important implications for the epidemiology and control of BVDV infection in the Gumushane region.

  İncele
• MakaleAçık Erişim2016Scopus SJRQ3/r/gumushane/11819
  Increased 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.

  • 
  AtıfScopus4·WoS4

  İncele
• MakaleAçık Erişim2016Scopus SJRQ3/r/gumushane/11597
  Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection

  Dincel, Gungor Cagdas; Atmaca, Hasan Tarik

  Oxidative stress (OS) plays an essential role in the pathogenesis of common neurodegenerative diseases. We have previously shown that Toxoplasma gondii (T. gondii) induces high nitric oxide (NO) production, glial activation, and apoptosis that altogether cause severe neuropathology in toxoplasma encephalitis (TE). The objective of this study was to investigate the cytotoxic effect of OS and to identify a correlation between the causes of T. gondii induced neuropathology. Expression levels of glutathione reductase (GR), Cu/Zn superoxide dismutase (SOD1), neuron specific enolase (NSE), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were investigated. Results of the study revealed that the levels of GR (P <0.005) and NSE (P <0.001) expression in the brain tissue markedly increased while SOD1 activity decreased (P <0.001) in the infected group compared to the non-infected group. In addition, intense staining for 8-OHdG (P <0.05) was observed both in the nucleus and the cytoplasm of neurons and glial cells that underwent OS. These results were reasonable to suggest that T. gondii-mediated OS might play a pivotal role and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of TE. The results also clearly indicated that increased levels of NO and apoptosis might contribute to OS-related pathogenesis of TE. As a result, OS and expression of NSE might give an idea of the disease progress and may have a critical diagnostic significance for patients with T. gondii infection.

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  AtıfScopus64·WoS55·OpenAlex62

  İncele
• MakaleYalnız künye2015Scopus SJRQ4/r/gumushane/15571
  Effectiveness of levamisole and tarantula cubensis extract in the treatment of teat Papillomatosis of cows

  Paksoy, Zahid; Gülesci, Nuri; Kandemir, Fatih Mehmet; Dinçel, Güngör Çagdas

  Papillomatosis is widespread in cattle and is often observed on the skin of udders. For treatment, anthelmintic, immunomodulator and homeopathic drugs are administered. The objective of the study was to examine the therapeutic effect of levamisole and tarantula cubensis extract in the treatment of papilloma observed in the teats of cows. Sixteen Holstein cows between the age of 2-3 years were used as study material. The cows with Papillomatosis were randomly assigned into two equal groups. The animals in the first group (n=8) were treated with intramuscular double doses of levamisole (5 mg/kg) applied one week apart. The second group of animals (n=8) was treated with two subcutaneous doses of 10 ml of Tarantula cubensis extract one week apart. Four animals in the first group recovered while 8 animals in the second group recovered. The total serum oxidant levels of the animals treated with Tarantula cubensis extract and levamisole on the 15th day was found to be significantly lower than the serum levels of same animals on day 0 of the treatment (P<0.05). The results of this study revealed that tarantula cubensis extract applied in normal therapeutic doses was more effective in the treatment of teat papillomatosis than levamisole.

  AtıfScopus7·WoS8

  İncele
• MakaleAçık Erişim2015Scopus SJRQ1/r/gumushane/15410
  Increased expressions of ADAMTS-13, neuronal nitric oxide synthase, and neurofilament correlate with severity of neuropathology in border disease virus-infected small ruminants

  Dincel, Gungor Cagdas; Kul, Oguz

  Border Disease (BD), caused by Pestivirus from the family Flaviviridae, leads to serious reproductive losses and brain anomalies such as hydranencephaly and cerebellar hypoplasia in aborted fetuses and neonatal lambs. In this report it is aimed to investigate the expression of neuronal nitric oxide synthase (nNOS), A Disintegrin And Metalloprotease with Throm-bospondin type I repeats-13 (ADAMTS-13), and neurofilament (NF) in the brain tissue in small ruminants infected with Border Disease Virus (BDV) and to identify any correlation between hypomyelinogenesis and BD neuropathology. Results of the study revealed that the levels of ADAMTS-13 (p<0.05), nNOS (p<0.05), and NF (p<0.05) were remarkably higher in BDV-infected brain tissue than in the uninfected control. It was suggested that L-arginine-NO synthase pathway is activated after infection by BDV and that the expression of NF and nNOS is associated with the severity of BD. A few studies have focused on ADAMTS-13 expression in the central nervous system, and its function continues to remain unclear. The most prominent finding from our study was that ADAMTS-13, which contain two CUB domains, has two CUB domains and its high expression levels are probably associated with the development of the central nervous system (CNS). The results also clearly indicate that the interaction of ADAMTS-13 and NO may play an important role in the regulation and protection of the CNS microenvironment in neurodegenerative diseases. In addition, NF expression might indicate the progress of the disease. To the best of the authors' knowledge, this is the first report on ADAMTS-13 expression in the CNS of BDV-infected small ruminants.

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  AtıfScopus15·WoS14·OpenAlex15

  İncele
• MakaleYalnız künye2015Scopus SJRQ2/r/gumushane/13157
  Nitric 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.

  • 
  AtıfScopus49·WoS44·OpenAlex53

  İncele
• MakaleYalnız künye2015Scopus SJRQ2/r/gumushane/13115
  eNOS and iNOS trigger apoptosis in the brains of sheep and goats naturally infected with the border disease virus

  Dincel, Gungor Cagdas; Kul, Oguz

  In this study, apoptotic and anti-apoptotic mechanisms and if present, which pathway to trigger the apoptosis in the brains of Border Disease Virus (BDV) infected lambs (n=10) and goat kids (n=5) were investigated. Briefly, apoptotic (caspase 3, caspase 9) and anti-apoptotic markers (Bcl-2), cytokine response (TNF-α, INF-γ), reactive gliosis and myelin loss were examined. eNOS, iNOS, caspase 9, caspase 3 and GFAP expressions were higher in BDV infected tissues compared to control animals (6 kids and 6 lambs) (p<0.05). Double immunoperoxidase test revelaed that TUNEL positive apoptotic cells showed significant association with increased eNOS-iNOS and iNOS-BDV expressions. However, no significant differences were found for TNFR1, TNF-α and INF-γ expressions in BD (p>0.05). There was a positive correlation between the intensity of myelin loss, GFAP activity and severity of infection. Inconclusion, as a novel finding, it is established that eNOS and iNOS overexpressions are coassociated with apoptosis in BDV infected neurons and neuroglia. The results also strongly suggested that BDV infected apoptotic cells mainly prefer the intrinsic pathway that might be most likely related to increased nitric oxide levels.

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  AtıfScopus16·WoS13·OpenAlex13

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