Person: ELİBOL, BİRSEN
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Publication Metadata only Mesenchymal stem cell therapy for the streptozotocin-induced neurodegeneration in rats(2016-01-01) Isik, Ahmet Turan; Celik, Turgay; URAL, Ali Ugur; Tosun, Murat; ULUSOY, Gokhan; Elibol, BİRSEN; ELİBOL, BİRSENBackground and Aim: Bone marrow-derived mesenchymal stem cells (BM-MSCs) are one of the sources of adult stem cells being explored for potential use in repairing neurodegenerative disorders. In this study, it was aimed to investigate the useful effects of BM-MSCs therapy on the streptozotocin-induced neurodegeneration in rats.Publication Metadata only Thymoquinone Can Improve Neuronal Survival and Promote Neurogenesis in Rat Hippocampal Neurons.(2018-03-01) Beker, M; Dallı, T; ELİBOL, BİRSENPublication Open Access High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions.(2018-10-15) Elibol, BİRSEN; KILIC, U; ELİBOL, BİRSENSIRT1 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.Publication Metadata only Thymoquinone activates MAPK pathway in hippocampus of streptozotocin-treated rat model(2018-03-01) Elibol, BİRSEN; Akbas, FAHRİ; dallı, Tugce; Terzioglu-Usak, ŞULE; Beker, MERVE; BEKER, MERVE; TERZİOĞLU, ŞULE; AKBAŞ, FAHRİ; ELİBOL, BİRSENStreptozotocin (STZ), a glucosamine-nitrosourea compound, produces deficiencies in learning, memory, and cognitive functions when it was administered intracerebroventricularly (i.c.v). In molecular level, increase in neuroinflammation and oxidative stress in brain, and decrease in the number of surviving neurons are the outcomes of STZ administration. Herein, we aimed to investigate the effect of thymoquinone (TQ), an anti-inflammatory, immunomodulatory and neuroprotective agent, on STZ-induced neurodegeneration in rats. For this purpose, bilateral i.c.v. injection of STZ (3 mg/kg) was given to adult female rats on days 1 and 3. TQ (20 mg/kg/day in cornoil) was administered intragastrically to rats for 15 days starting from the 15th day of STZ injection. The Morris water maze test and passive avoidance test were applied to measure the learning and memory performance of animals. Following the behavioral tests, all of the rats were sacrificed for evaluation of molecular alterations. Rats in the STZ-TQ group showed higher performance in passive avoidance test than rats in the STZ group whose memory performance declined compared to control group. The worse memory performance in STZ group was correlated with low number of surviving neurons and high number of degenerating neurons. In addition, an increase in APOE expression and a decrease in NGF expression were observed with STZ injection. Administration of TQ reversed these STZ-triggered cognitive and molecular alterations. In the present study, we observed the neuroregenerative effects of TQ by activation of JNK protein, upregulation of mir-124, and downregulation of ERK1/2 and NOS enzymes. The same ameliorative effect of TQ was also observed in the pTau protein expression. To sum up, we can say that the healing effect of TQ on STZ induced neurodegeneration opens a new door for the development of Alzheimer-s disease treatment using natural products as an adjuvant when their action mechanism was explained in detail.Publication Metadata only Specific alterations in the circulating levels of the SIRT1, TLR4, and IL7 proteins in patients with dementia(2018-10-01) Yildiz, Gulsen Babacan; kılıç, Ulkan; Elibol, BİRSEN; Uysal, Omer; Kilic, Ertugrul; Yulug, Burak; Sakul, Arzu Sayin; ELİBOL, BİRSEN; UYSAL, ÖMER; BABACAN YILDIZ, GÜLSENSirtuins have gained considerable attention as epigenetic regulators for slowing aging and age-related disorders. The growing association between neurodegeneration and inflammation has led researchers to investigate interactions of sirtuins with inflammatory markers in neurodegenerative diseases. We analyzed SIRT1-s association with chronic inflammation in dementia as an age-related neurodegenerative condition through Toll-like receptor 4 (TLR4) and interleukin-7 (IL7) for the first time. In the present study, we observed a significant increase in the level of SIRT1 in patients with all types of dementia. Interestingly, the level of TLR4 protein was significantly lower in only the patients with Alzheimer-s disease (AD) compared to the healthy elderly subjects. There was no significant change in the level of IL7 between the diseased and healthy elderly subjects. A significant positive correlation between SIRT1 level and age in healthy elderly subjects was evident according to Pearson-s correlation test. However, this correlation was not observed in the dementia patients. Furthermore, the positive correlation between the levels of IL7 and TLR4 in the healthy elderly subjects was absent in the dementia patients. However, there was no direct association between the examined single nucleotide polymorphisms (SNPs) and dementia at the molecular level. According to logistic regression analysis, dementia risk increases 1.16 times due to an increase in the SIRT1 level and 24.23 times due to a decrease in the TLR4 level. Interestingly, a high level in the total antioxidant status (TAS) increases the risk of dementia approximately 33.32 times. Therefore, the current study, for the first time, provides a much better molecular understanding of the interaction between decreasing TLR4 levels and increasing SIRT1 levels in dementia, especially in AD. Furthermore, it highlights the importance of epigenetics in several age-related diseases and suggests that developing novel therapies to prevent or slow down the progression of dementia may support healthy aging.Publication Open 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 DILEKIt 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.Publication Open Access Prenatal exposure of diclofenac sodium alters the behavioral development of young Wistar rats.(2019-10-14) Elibol, BİRSEN; Aritan, Oğur; Doğru, H; ELİBOL, BİRSENDiclofenac 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.Publication Metadata only Effects of prenatal binge-like ethanol exposure and maternal stress on postnatal morphological development of hippocampal neurons in rats.(2017-10-01) Jakubowska-Dogru, E; Elibol, BİRSEN; Dursun, I; Yürüker, S; ELİBOL, BİRSEN