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Başlık: Uridine protects against hypoxic-ischemic brain injury by reducing histone deacetylase activity in neonatal rats
Yazarlar: Çetinkaya, Merih
Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı.
0000-0001-8061-8756
0000-0003-2918-5064
0000-0001-6466-5042
Koyuncuoğlu, Türkan
Türkyımaz, Mesut
Gören, Bülent
Cansev, Mehmet
Alkan, Tülin
O-9601-2015
EBA-0754-2022
AAH-1718-2021
M-9071-2019
AAH-1792-2021
57190272398
56320252500
6602543716
8872816100
6601953747
Anahtar kelimeler: Neurosciences & neurology
Hypoxic-ischemic encephalopathy
Neonatal
Rat
Uridine
Histone deacetylase
Neuroprotection
Docosahexaenoic acid
CDP-choline
Inhibition
Model
Combination
Damage
Neurodegeneration
Neuroprotection
Mechanisms
Receptors
Yayın Tarihi: 5-Eki-2015
Yayıncı: IOS Press
Atıf: Koyuncuoğlu, T. vd. (2015). "Uridine protects against hypoxic-ischemic brain injury by reducing histone deacetylase activity in neonatal rats". Restorative Neurology and Neuroscience, 33(5), 777-784.
Özet: Purpose: A significant cause of neurological disability in newborns is hypoxic-ischemic encephalopathy (HIE), a disorder which involves an enhancement in histone deacetylase (HDAC) activity among underlying pathological mechanisms. We showed recently that exogenous administration of uridine to newborn rats with HIE reduced brain injury in a dose-dependent manner. The present study was performed to investigate whether uridine modulates histone acetylation/deacetylation balance in a neonatal rat model of HIE. Methods: Newborn rats that were subjected to hypoxic-ischemic (HI) insult on postnatal day 7 (P7) were injected intraperitoneally with either saline or uridine (500 mg/kg) for three consecutive days. One day after completion of treatment, brains of pups were collected for evaluation of brain infarct volume, apoptosis, HDAC activity and acetylated-Histone H3 (Ac-H3) and H4 (Ac-H4) protein levels. Results: Results revealed that uridine administration reduced infarct volume, active Caspase-3 levels and HDAC activity while increasing the expressions of Ac-H3 and Ac-H4 proteins. Conclusions: We conclude that one mechanism by which uridine provides neuroprotection in neonatal rat HIE model involves reduction in HDAC activity.
URI: https://content.iospress.com/articles/restorative-neurology-and-neuroscience/rnn150549
https://doi.org/10.3233/RNN-150549
http://hdl.handle.net/11452/34372
ISSN: 0922-6028
Koleksiyonlarda Görünür:Scopus
Web of Science

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