Person: ELİBOL, BİRSEN
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Publication Metadata only Effects of Angiotensin IV on Learning-Memory and Hippocampal Oxidative Stress in Diabetic Rats(2019-12-01T00:00:00Z) KILIÇ, Aysu; ÜSTÜNOVA, SAVAŞ; ELİBOL, BİRSEN; Bulut, Huri; MERAL, İSMAİL; Sahin, Emine Gulderen; KILIÇ, AYSU; ÜSTÜNOVA, SAVAŞ; ELİBOL, BİRSEN; BULUT, HURI; MERAL, İSMAİLPublication Metadata only SIRT1 gene variants are related to risk of childhood obesity(2015-04-01) Kilic, Ulkan; GOK, Ozlem; ELIBOL-CAN, BİRSEN; Ozgen, Ilker Tolga; Erenberk, UFUK; Uysal, Omer; DUNDAROZ, Mehmet Rusen; ELİBOL, BİRSEN; ÖZGEN, İLKER TOLGA; ERENBERK, UFUK; UYSAL, ÖMERObesity is a multifactorial disorder resulting from the interaction between genetic, psychological, physical, environmental, and socioeconomic factors. SIRT1 gene has important effects on the regulation of adiponectin, caloric restriction, insulin sensitivity, coronary atherosclerosis, and cardiovascular diseases. The aim of this study was to investigate the association between childhood obesity and SIRT1 gene polymorphisms regarding rs7895833 A > G in the promoter region, rs7069102 C > G in intron 4, and rs2273773 C > T in exon 5 using PCR-CTPP method in 120 obese and 120 normal weight children. In this study, BMI, systolic and diastolic blood pressure, LDL cholesterol, triglyceride, and insulin levels were significantly higher and HDL-cholesterol levels were significantly lower in obese children compared to normal weight children. For rs7895833 A > G, the rate of having AG genotype and G allele was significantly higher in obese children compared to non-obese group (p T. There was no significant difference for rs7069102 C > G gene polymorphism between groups.Publication Metadata only Both activation and inhibition of SIRT1 may act via exosomal GSK3α/β in the in vitro amyloid beta toxicity model(2019-12-01) Elibol, Birsen; ELİBOL, BİRSENPublication 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 Metadata only Examination of Age-dependent effects of fetal ethanol exposure on behavior, hippocampal cell counts, and doublecortin immunoreactivity in rats(2014-05-01T00:00:00Z) Elibol-Can, BİRSEN; Dursun, Ilknur; Telkes, Ilknur; Kilic, Ertugrul; Canan, Sinan; Jakubowska-Dogru, Ewa; ELİBOL, BİRSENEthanol is known as a potent teratogen having adverse effects on brain and behavior. However, some of the behavioral deficits caused by fetal alcohol exposure and well expressed in juveniles ameliorate with maturation may suggest some kind of functional recovery occurring during postnatal development. The aim of this study was to reexamine age-dependent behavioral impairments in fetal-alcohol rats and to investigate the changes in neurogenesis and gross morphology of the hippocampus during a protracted postnatal period searching for developmental deficits and/or delays that would correlate with behavioral impairments in juveniles and for potential compensatory processes responsible for their amelioration in adults. Ethanol was delivered to the pregnant dams by intragastric intubation throughout 7-21 gestation days at daily dose of 6 g/kg. Isocaloric intubation and intact control groups were included. Locomotor activity, anxiety, and spatial learning tasks were applied to juvenile and young-adult rats from all groups. Unbiased stereological estimates of hippocampal volumes, the total number of pyramidal and granular cells, and double cortin expressing neurons were carried out for postnatal days (PDs) PD1, PD10, PD30, and PD60. Alcohol insult during second trimester equivalent caused significant deficits in the spatial learning in juvenile rats; however, its effect on hippocampal morphology was limited to a marginally lower number of granular cells in dentate gyrus (DG) on PD30. Thus, initial behavioral deficits and the following functional recovery in fetal-alcohol subjects may be due to more subtle plastic changes within the hippocampal formation but also in other structures of the extended hippocampal circuit. Further investigation is required. (c) 2013 Wiley Periodicals, Inc. Develop Neurobiol 74: 498-513, 2014Publication Metadata only Delayed Therapeutic Administration of Melatonin Enhances Neuronal Survival Through AKT and MAPK Signaling Pathways Following Focal Brain Ischemia in Mice(2022-03-01T00:00:00Z) Kilic, Ulkan; ELİBOL, BİRSEN; ÇAĞLAYAN, AHMET BURAK; Beker, Mustafa Caglar; Beker, Merve; Altug-Tasa, Burcugul; UYSAL, ÖMER; YILMAZ, BAYRAM; KILIÇ, ERTUĞRUL; ELİBOL, BİRSENMelatonin has a role in the cell survival signaling pathways as a candidate for secondary stroke prevention. Therefore, in the present study, the coordination of ipsilateral and contralateral hemispheres to evaluate delayed post-acute effect of melatonin was examined on recovery of the cell survival and apoptosis after stroke. Melatonin was administered (4 mg/kg/day) intraperitoneally for 45 days, starting 3 days after 30 min of middle cerebral artery occlusion. The genes and proteins related to the cell survival and apoptosis were investigated by immunofluorescence, western blotting, and RT-PCR techniques after behavioral experiments. Melatonin produced delayed neurological recovery by improving motor coordination on grip strength and rotarod tests. This neurological recovery was also reflected by high level of NeuN positive cells and low level of TUNEL-positive cells suggesting enhanced neuronal survival and reduced apoptosis at the fifty-fifth day of stroke. The increase of NGF, Nrp1, c-jun; activation of AKT; and dephosphorylation of ERK and INK at the fifty-fifth day showed that cell survival and apoptosis signaling molecules compete to contribute to the remodeling of brain. Furthermore, an increase in the CREB and Atf-1 expressions suggested the melatonin-s strong reformative effect on neuronal regeneration. The contralateral hemisphere was more active at the latter stages of the molecular and functional regeneration which provides a further proof of principle about melatonin-s action on the promotion of brain plasticity and recovery after stroke.Publication Metadata only Inflammatory Cytokines are in Action: Brain Plasticity and Recovery after Brain Ischemia Due to Delayed Melatonin Administration.(2021-09-18T00:00:00Z) Kilic, Ulkan; Elibol, BİRSEN; Beker, Merve; Altug-Tasa, Burcugul; Caglayan, Ahmet Burak; Beker, Mustafa Caglar; Yilmaz, Bayram; Kilic, Ertugrul; ELİBOL, BİRSENPublication Metadata only Effects of fetal alcohol and maternal intubation stress on the expression of proteins controlling postnatal development of male rat hippocampus(2020-09-01T00:00:00Z) ELİBOL, BİRSEN; BEKER, MERVE; KILIÇ, ÜLKAN; Jakubowska-Dogru, Ewa; ELİBOL, BİRSEN; BEKER, MERVEBackground Developing brains can partially get over prenatal alcohol exposure-related detrimental conditions by activating some mechanisms involved in survival. Objectives This study aimed to shed light on the molecular correlates of compensatory mechanisms by examining temporal profiles in the expression of proteins controlling postnatal development in the rat hippocampus prenatally exposed to intubation stress/ethanol. Methods Male pups were randomly assigned to age subgroups (n = 21/age) which were sacrificed on postnatal day (PD)1, PD10, PD30, and PD60. Ethanol (6 g/kg/day) were intragastrically intubated to the dams throughout 7-21 gestation days. The expression of neurogenesis and angiogenesis markers, extracellular matrix proteins, and growth-promoting ligands were examined by western blot. Results The most rapid increase in the index of neuronal maturation was noted between PD10-PD30 (p< .05). Prenatal stress caused a decrease of neurogenesis markers at birth and an increase of their expressions at PD10 and PD30 to reach control levels (p< .001). The impact of fetal-alcohol was observed as a decrease in the expression of synaptic plasticity protein versican at birth (p< .001), an increase in the synaptic repulsion protein ephrin-B2 at PD10 (p< .001), and a decrease in the maturation of BDNF at PD30 (p< .001) with a decrease in the mature neuron markers at PD30 (p< .001) and PD60 (p= .005) which were compensated with upregulation of angiogenesis and increasing brevican expression, a neuronal maturation protein (p< .001). Conclusion These data providein vivoevidence for the potential therapeutic factors related to neurogenesis, angiogenesis, and neurite remodeling which may tolerate the alcohol/stress dependent teratogenicity in the developing hippocampus.Publication 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.