Person:
ELİBOL, BİRSEN

Profile Picture
Google ScholarScopusORCIDPublons
Status
Kurumdan Ayrılmıştır
Organizational Units
OrgUnit Logo
Organizational Unit
Job Title
First Name
BİRSEN
Last Name
ELİBOL
Name
Email Address
Birth Date

Filters

2018 - 20204
Reset filters

Settings

Item Type: Publication × Rights: info:eu-repo/semantics/openAccess × Author: Elibol, BİRSEN ×

Search Results

Now showing 1 - 4 of 4
  • Thumbnail Image
    PublicationOpen Access
    High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions.
    (2018-10-15) Elibol, BİRSEN; KILIC, U; ELİBOL, BİRSEN
    SIRT1 protein, a member of Silent Information Regulator 2 (Sir2) protein family, have gained considerable attention as epigenetic regulators for a great area in the human physiology. Changes in sirtuin expression are critical in several diseases, including metabolic syndrome, cardiovascular diseases, cancer and neurodegeneration. Here, we provide an overview of the association of the increasing level of SIRT1 protein for regulating some disease related conditions such as obesity, cardiovascular diseases and neurodegeneration. This review also provides a detailed molecular understanding of the interaction of the some basic molecules with increasing SIRT1 levels rather than reduction of the SIRT1 expression. In this context, the current approaches to enhancing the expression of SIRT1 points the importance of epigenetics in several age-related diseases to provide a healthy aging by developing novel therapies which can prevent or damp the progression of some diseases.
  • Thumbnail Image
    PublicationOpen Access
    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.
  • Thumbnail Image
    PublicationOpen Access
    Prenatal exposure of diclofenac sodium alters the behavioral development of young Wistar rats.
    (2019-10-14) Elibol, BİRSEN; Aritan, Oğur; Doğru, H; ELİBOL, BİRSEN
    Diclofenac sodium (DS), a potent inhibitor of cyclooxygenase, reduces the release of arachidonic acid and formation of prostaglandins. Being a nonsteroid drug that shows antiinflammatory action, the possible side effects of fetal DS administration gain importance in public and medical applications. Herein, the effects of DS administration (1 mg/kg) during gestational days 5–20 were investigated on the performance of Wistar rat pups in a variety of behavioral tasks. Four-week-old pups were subjected to sensory motor tests, a plus maze, an open field, the Morris water maze, and a radial arm maze. Fetal DS disrupted some sensory motor performances, such as visual placing and climbing in both females and males. In the open field, DS females had a higher level of anxiety and male DS pups habituated to the environment slowly compared to controls. The DS pups showed slower rates of learning, whereas no substantial between-group differences were found in the performance of spatial memory compared to both controls. Furthermore, working memory was negatively affected by fetal DS. In conclusion, it was indicated that DS administration during pregnancy had slight behavioral impacts with a delay in learning and a defect in the short-term memory in juvenile rats.
  • Thumbnail Image
    PublicationOpen Access