Person:
ŞAHBAZ, ÇIĞDEM DILEK

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ÇIĞDEM DILEK
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ŞAHBAZ
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Author: ELİBOL, BİRSEN ×

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    Necroptosis Might be a Time Dependent Neuronal Cell Death Mechanism on Hippocampus After Chronic Restraint Stress
    (2019-05-15) Sahbaz, Cigdem; ELİBOL, BİRSEN; ŞAHBAZ, ÇIĞDEM DILEK; ELİBOL, BİRSEN
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    Thymoquinone (TQ) demonstrates its neuroprotective effect via an anti-inflammatory action on the Aβ(1–42)-infused rat model of Alzheimer-s disease
    (2019-10-01) Elibol, Birsen; Şahbaz, Çiğdem Dilek; Beker, Merve; Terzioğlu, Şule; ELİBOL, BİRSEN; TERZİOĞLU, ŞULE; BEKER, MERVE; ŞAHBAZ, ÇIĞDEM DILEK
    OBJECTIVES: Alzheimer-s disease (AD) is a severe neurodegenerative disease with presentation of the neuronal death, memory loss and cognitive decline. The relationship between neuroinflammation and AD has been well documented. However, the options of anti-inflammatory treatment are very limited in patients with AD. Previous studies showed that flavonoids might be an effective treatment and thymoquinone (TQ), an aromatic hydrocarbon found in Nigella sativa suggested as a candidate molecule due to having strong anti-inflammatory effects. Our study aimed to investigate the effects of TQ on neuroinflammation and neuroprotection in A beta((1-42)) infused rat model of AD.
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    Prenatal ethanol intoxication and maternal intubation stress alter cell survival and apoptosis in the postnatal development of rat hippocampus.
    (2019-01-01) Sahbaz, CD; Elibol, BİRSEN; Beker, M; Kilic, U; Jakubowska-Doğru, E; ELİBOL, BİRSEN; ŞAHBAZ, ÇIĞDEM DILEK
    It is well known that the fetal ethanol exposure and prenatal stress may have adverse effects on brain development. Interestingly, some morphological and functional recovery from their teratogenic effects that take place during brain maturation. However, mechanisms that underlie this recovery are not fully elucidated. The aim of this study was to examine whether the postnatal attenuation of fetal alcohol - and maternal stress‑induced morphological and functional deficits correlates with compensatory changes in the expression/activation of the brain proteins involved in inflammation, cell survival and apoptosis. In this project, we investigated the hippocampus which belongs to the brain regions most susceptible to the adverse effects of prenatal ethanol exposure. Pregnant rat dams were administered ethanol (A) or isocaloric glucose solution (IC) by a gastric intubation during gestational days 7-20. The pure control group received ad libitum laboratory chow and water with no other treatment. The hippocampi of fetal-ethanol and control pups were examined at the postnatal day (PD)1, PD10, PD30 and PD60. Moderate fetal-ethanol exposure and prenatal intubation stress caused a significant increase in molecular factors relating to inflammation (iNOS) and cell survival/apoptosis pathways (PTEN, GSK-3 and ERK) at birth, with a rapid compensation from these developmental deficits upon removal of alcohol at PD10. Indeed, an increase in ERK1/2 and JNK1/2 activation at PD30 was observed with ethanol consumption. It indicates that the recovery process in A and IC brains started soon after the birth upon the ethanol and stressor withdrawal and continued until the adulthood.