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    Changes in als2 expression leads to different outcomes on the expression of two NF-kB targeted genes in N2a and C2C12 cell lines
    (Logos Medical Publishing, 2019) Ozansoy, Mehmet; Ozansoy, Muzaffer Beyza
    Objective: Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disorder affecting spinal and cortical motor neurons. Motor neuron degeneration leads to progressive muscular atrophy. Als2 (alsin) is one of the causative genes of ALS and UXT gene is an interacting partner of Als2. Since UXT is a known cofactor in NF-?B enhancesome, we aimed here to compare the effects of Als2 silencing on NF-?B activity by using N2a and C2C12 cell lines. Methods: Mouse neuroblastoma cells (N2a) and myoblast cell lines (C2C12) were used. Als2 was silenced by RNAi and UXT, A20 and IL8 expressions were measured by qRT-PCR. Data were statistically evaluated by Student t-test. Results: A 73.4% decrease was observed in Als2 expression in N2a cells, whereas 73.7% decrease in the C2C12 cells was found. UXT expression in Als2-silenced N2a cells was found to be decreased by 40%, while a 9-fold increase in C2C12 cells was detected. IL8 expression demonstrated a 84% decrease in N2a cells. On the other hand,IL8 expression increased 50-fold in C2C12 cells. A20 expression increased by 65% in N2a cell line, and increased 10 fold in C2C12 cell line. Conclusion: We have concluded that silencing Als2 gene over UXT on exerts different effects on NF-?B pathway We arrived at this conclusion because changes in the expressions of the IL8 and A20 genes differ in both cell lines. In addition, the link between Als2 and UXT is shown again in both cell lines and it is understood that the silencing Als2 may give rise to different results as for neuronal cells and muscle cells.
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    Melatonin affects the release of exosomes and tau-content in in vitro amyloid-beta toxicity model
    (Elsevier Science Ltd., 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 beta toxicity model.Method: SH-SY5Y cell line was used. The optimum concentration of A beta was determined by cell viability and cell proliferation tests. Melatonin (100 mM) was applied before and after A beta 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 beta 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.
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    The effect of rifampicin on the neuronal cell survival in primary cortical neuron culture after laser axotomy
    (2019) Ozansoy, Mehmet; Coşkun, Ebru; Ozansoy, Muzaffer Beyza; Çankaya, Şeyda; Günal, Mehmet Yalçın; Bayraktaroğlu, Zübeyir; Yuluğ, Burak; 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.
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    The potential role of boron in the modulation of gut microbiota composition: an in vivo pilot study
    (2024) Şentürk, Nermin Başak; Kasapoğlu, Burcu; Şahin, Eray; Özcan, Orhan; Ozansoy, Mehmet; Ozansoy, Muzaffer Beyza; Şahin, Fikrettin
    Background/Objectives: The role of the gut microbiome in the development and progression of many diseases has received increased attention in recent years. Boron, a trace mineral found in dietary sources, has attracted interest due to its unique electron depletion and coordination characteristics in chemistry, as well as its potential role in modulating the gut microbiota. This study investigates the effects of inorganic boron derivatives on the gut microbiota of mice. Methods: For three weeks, boric acid (BA), sodium pentaborate pentahydrate (NaB), and sodium perborate tetrahydrate (SPT) were dissolved (200 mg/kg each) in drinking water and administered to wild-type BALB/c mice. The composition of the gut microbiota was analyzed to determine the impact of these treatments. Results: The administration of BA significantly altered the composition of the gut microbiota, resulting in a rise in advantageous species such as Barnesiella and Alistipes. Additionally, there was a decrease in some taxa associated with inflammation and illness, such as Clostridium XIVb and Bilophila. Notable increases in genera like Treponema and Catellicoccus were observed, suggesting the potential of boron compounds to enrich microbial communities with unique metabolic functions. Conclusions: These findings indicate that boron compounds may have the potential to influence gut microbiota composition positively, offering potential prebiotic effects. Further research with additional analyses is necessary to fully understand the interaction between boron and microbiota and to explore the possibility of their use as prebiotic agents in clinical settings.
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    Two boron-containing compounds affect the cellular viability of SH-SY5Y cells in an in vitro amyloid-beta toxicity model
    (Scientific and Technological Research Council of Turkey (TÜBİTAK), 2020) Ozansoy, Mehmet; Altıntaş, Mehmet Özgen; Ozansoy, Muzaffer Beyza; Günay, Necmeddin; Kılıç, Ertuğrul; Kılıç, Ülkan
    Boron is a naturally occurring trace element found in organic and inorganic complexes. Boron-containing compounds are required for living organisms for diverse metabolic functions, including nitrogen fixation in microorganisms, cell wall stability in plants, and bone and carbohydrate metabolism in animals. The number of studies about the effect of boron in biological model systems is very limited; so far, there has been no study on the correlation between boron and amyloid-beta toxicity. Here, we investigated the possible effects of 2 boron-containing compounds-sodium borate decahydrate and boric acid-against amyloid-beta toxicity. In our in vitro amyloid-beta toxicity model, we showed that these 2 compounds increase the survival of the SH-SY5Y cells. Furthermore, boron in these 2 forms increases the expression of Sirt1, which has protective functions against cellular stress. The compounds also change the expressions of GSK-3 alpha/beta; by doing so, boron may contribute to the stimulation of intracellular prosurvival pathways. This is the first experimental study indicating the prosurvival effect of boron in an amyloid-beta toxicity model.