Uridine protects against hypoxic-ischemic brain injury by reducing histone deacetylase activity in neonatal rats

KOYUNCUOĞLU T., Turkyilmaz M., GÖREN B., Cetinkaya M., CANSEV M., ALKAN T.

RESTORATIVE NEUROLOGY AND NEUROSCIENCE, vol.33, no.5, pp.777-784, 2015 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 33 Issue: 5
  • Publication Date: 2015
  • Doi Number: 10.3233/rnn-150549
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.777-784
  • Keywords: Hypoxic-ischemic encephalopathy, neonatal, rat, uridine, histone deacetylase, neuroprotection, DOCOSAHEXAENOIC ACID, CDP-CHOLINE, INHIBITION, MODEL, COMBINATION, DAMAGE, NEURODEGENERATION, NEUROPROTECTION, MECHANISMS, RECEPTORS
  • Bursa Uludag University Affiliated: Yes


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.