Uridine treatment protects against neonatal brain damage and long-term cognitive deficits caused by hyperoxia

Autor: Mehmet Cansev, Sema Serter Kocoglu, Cansu Sevinc, Ceren Oy, Busra Ocalan, Zehra Minbay, Tulin Alkan, Aysen Cakir, Bulent Goren, Nevzat Kahveci
Přispěvatelé: Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı., Uludağ Üniversitesi/Tıp Fakültesi/Eczacılık Anabilim Dalı., Uludağ Üniversitesi/Tıp Fakültesi/Histoloji ve Embriyoloji Anabilim Dalı., Gören, Bülent, Çakır, Aysen, Sevinç, Cansu, Koçoğlu, Sema Serter, Öçalan, Buşra, Oy, Ceren, Minbay, Zehra, Kahveci, Nevzat, Alkan, Tülin, Cansev, Mehmet, AAH-1792-2021, AAL-1786-2020, AAG-7070-2021, AAH-4278-2021, ABC-1475-2020, AAA-4754-2022, AAH-1718-2021, M-9071-2019, A-6819-2018, N-9927-2019
Rok vydání: 2017
Předmět:
Induced cell-death
Male
Newborn disease
Injury
Apoptosis
Cell Count
Pathogenesis
Cytidine
Hippocampal CA3 region
Rats
Sprague-Dawley
Cognition
Hippocampal CA1 region
0302 clinical medicine
Pathology
Psychology
Brain injury
Myelin Sheath
Neurons
Hyperoxia
Learning Disabilities
Brain
Cognitive defect
Beta tubulin
medicine.medical_specialty
Oxygen consumption
Brain damage
Article
03 medical and health sciences
Memory
Reflex
Animal model
Cognitive Dysfunction
Animal experiment
Molecular Biology
Behavior
Animal
Disease model
Oxygen therapy
Uridine
Oxygen
Drug effect
Myelin basic protein
030104 developmental biology
Endocrinology
Postnatal care
chemistry
Coordination
Brain Injuries
Rat
Neurology (clinical)
030217 neurology & neurosurgery
Developmental Biology
0301 basic medicine
Randomization
medicine.disease_cause
Myelination
Random Allocation
chemistry.chemical_compound
Priority journal
Sensorimotor function
Oligodendrocytes
Caspase 3
General Neuroscience
Learning disorders
Volumes
Nerve cell
Ambient air
Neuroprotection
Sprague dawley rat
Neuroprotective Agents
medicine.anatomical_structure
Newborn period
Learning disorder
Anesthesia
Rat model
Neonatal rat
Female
medicine.symptom
Cell death
Pup (rodent)
Cell Survival
Sodium chloride
Growth
development and aging
Inflammation
Neurosciences & neurology
Pathophysiology
Learning and memory
Internal medicine
medicine
Learning
Animals
Erythropoietin
Cibinetide
Darbepoetin Alfa
business.industry
Neurosciences
Neuroprotective agent
Water-maze
Newborn
Nonhuman
Disease Models
Animal
Animals
Newborn
Neuron
business
Controlled study
Oxidative stress
Zdroj: Brain Research. 1676:57-68
ISSN: 0006-8993
DOI: 10.1016/j.brainres.2017.09.010
Popis: Exposure to excessive oxygen in survivors of preterm birth is one of the factors that underlie the adverse neurological outcome in later life. Various pathological changes including enhanced apoptotic activity, oxidative stress and inflammation as well as decreased neuronal survival has been demonstrated in animal models of neonatal hyperoxia. The aim of the present study was to investigate the effect of administering uridine, an anti-apoptotic agent, on cellular, molecular and behavioral consequences of hyperoxia-induced brain damage in a neonatal rat model. For five days from birth, rat pups were either subjected continuously to room air (21% oxygen) or hyperoxia (80% oxygen) and received daily intraperitoneal (i.p.) injections of saline (0.9% NaCl) or uridine (500 mg/kg). Two-thirds of all pups were sacrificed on postnatal day 5 (P5) in order to investigate apoptotic cell death, myelination and number of surviving neurons. One-thirds of pups were raised through P40 in order to evaluate early reflexes, sensorimotor coordination and cognitive functions followed by investigation of neuron count and myelination. We show that uridine treatment reduces apoptotic cell death and hypomyelination while increasing the number of surviving neurons in hyperoxic pups on P5. In addition, uridine enhances learning and memory performances in periadolescent rats on P40. These data suggest that uridine administered during the course of hyperoxic insult enhances cognitive functions at periadolescent period probably by reducing apoptotic cell death and preventing hypomyelination during the neonatal period in a rat model of hyperoxia-induced brain injury.
Databáze: OpenAIRE
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