Yazar "Ozansoy, Muzaffer Beyza" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • [ X ]
    Öğe
    Melatonin affects the release of exosomes and tau-content in in vitro amyloid-beta toxicity model
    (Churchill Livingstone, 2020) Ozansoy, Mehmet; Ozansoy, Muzaffer Beyza; Yuluğ, Burak; Çankaya,Şeyda; Kılıç, Ertuğrul; Göktekin, Şule; Kılıç, Ülkan
    Background: Recent studies have been revealed that oxidative damage is the main cause of aging and age-related neurodegenerative diseases like Alzheimer's disease (AD). Melatonin is secreted from the pineal gland and its secretion has been found to be altered in AD. In the last decade the role of exosomes in spreading toxic proteins and inducing the propagation of diseases like AD has been discussed. However, it is not known how melatonin affects the amount of exosomes released from the cells and the content of the exosomes. Objective: Herein, we investigated the possible role of melatonin treatment in the releasing of exosomes and exosomal tau content in an in vitro A? toxicity model. Method: SH-SY5Y cell line was used. The optimum concentration of A? was determined by cell viability and cell proliferation tests. Melatonin (100 µM) was applied before and after A? application. Total exosomes isolated from cell culture media were immunoprecipitated. The amount of released exosomes and their tau content were analyzed by Western blots. Results: Our data demonstrated for the first time that melatonin treatment clearly affected the amount of released exosomes. It would decrease the amyloid beta load and toxicity by inhibiting exosome release. We also demonstated that melatonin also affected the level of tau carried by exosomes depending on whether melatonin was applied before or after A? application. Conclusion: It is considered that the effect of melatonin in the release of exosomes and exosomal tau content would contribute the development of therapeutic strategies in AD and related disorders. © 2019 Elsevier Ltd
  • [ X ]
    Öğe
    The effect of rifampicin on the neuronal cell survival in primary cortical neuron culture after laser axotomy
    (Alanya Alaaddin Keykubat Üniversitesi, 2019) Ozansoy, Mehmet; Coşkun, Ebru; Ozansoy, Muzaffer Beyza; Çankaya, Şeyda; Günal, Mehmet Yalçın; Bayraktaroğlu, Zübeyir; Hanoğlu, Lütfü
    Aim: Neurodegeneration caused by the axonal injury is a widely seen phenomenon in spinal cord and traumatic brain injuries. Due to the disintegration of the synaptic connection neurotrophic factors could not be transported retrogradely towards the cell body and the deprivation of the trophic factors lead to the degeneration and death of the injured neuron. Rifampicin is an antibiotic exhibiting several neuroprotective functions in various neurodegenerative conditions. Here we aim to investigate the acute neuroprotective effect of rifampicin in primary cortical neuron culture in which neurons are axotomized by laser axotomy. Methods: Neonatal male mice were used in order to isolate cortical neurons. Isolated primary cortical neurons were cultured. After 24 hours three different rifampicin concentrations (1 µM, 10 µM and 100 µM) were applied to the neurons and after 15 minutes of rifampicin addition, neurons were laser axotomized. Viability of the cells was evaluated by propidium iodide staining after 24 hours of axotomy. Results: Laser axotomy decreases the cortical neuron viability significantly by 80.45%, while rifampicin pre-treatment increases their viability in all three dosages in a statistically significant manner. Conclusion: Rifampicin has an acute neuroprotective effect on the viability of the laser axotomized cortical neurons.