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

Gören, Bülent; Çakır, Ayşen; Sevinc, Cansu; Koçoğlu, Sema Serter; Öcalan, Büşra; Oy, Ceren; Minbay, Zehra; Kahveci, Nevzat; Alkan, Tülin; Cansev, Mehmet

doi:10.1016/j.brainres.2017.09.010

Cited by 17 publications

(13 citation statements)

References 45 publications

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“…These data show that uridine exhibits antioxidative properties in a neonatal rat model of hyperoxic brain damage suggesting one mechanism by which uridine provides neuroprotection in such model [28]. We showed, for the first time, that a single dose of uridine injected to P6 pups prevented the hyperoxia-induced decreases in SOD and GSH-Px levels as well as the hyperoxia-induced increases in MDA and MPO levels, in a dose-dependent manner.…”

Section: Discussionsupporting

confidence: 53%

“…Normoxia+Saline group, ## P < 0.01 and ### P < 0.001 compared to Hyperoxia+Saline group. reduced apoptosis in pups' brains and protected against long-term cognitive deficits [28]. Although uridine has been shown to exhibit antiinflammatory effects in models of pulmonary diseases [53,54] or colitis [55], the effect of uridine on oxidative stress has not yet been studied.…”

Section: Discussionmentioning

confidence: 99%

“…Saline (0.9% NaCl; 0.1 ml/10 g body weight) or uridine (100 mg/kg, 300 mg/ kg, or 500 mg/kg; dissolved in saline) was administered intraperitoneally (i. p.) once 15 min before the onset of atmospheric air or oxygen exposure. Doses of uridine administered in this study were selected from our previous studies reporting neuroprotective effects in neonatal rat models of hypoxic-ischemic encephalopathy [25][26][27] and hyperoxic brain injury [28]. The oxygen level inside the chamber was monitored continuously with a MiniOX 3000 oxygen analyzer (Ohio Medical Corporation, Gurnee, IL, USA) to maintain 80% oxygen saturation.…”

Section: Induction Of Hyperoxic Brain Injurymentioning

confidence: 99%

“…Uridine is the principal circulating pyrimidine nucleoside in human circulation [21,22], a constituent of breast milk [23], and a precursor of brain membrane phospholipids via the Kennedy pathway [24]. We showed previously that exogenously administered uridine provides neuroprotection in neonatal rat models of hypoxic-ischemic encephalopathy (HIE) [25][26][27] and hyperoxic brain injury [28]. The neuroprotection by uridine has been shown to be mediated by its antiapoptotic [25] and epigenetic effects (i.e., reducing histone deacetylase activity) [27] in the neonatal HIE model.…”

Section: Introductionmentioning

confidence: 99%

“…The neuroprotection by uridine has been shown to be mediated by its antiapoptotic [25] and epigenetic effects (i.e., reducing histone deacetylase activity) [27] in the neonatal HIE model. Hence, for the first time, the present study aimed to investigate the mechanism by which uridine exhibited neuroprotection in the neonatal rat model of hyperoxic brain injury [28] with regard to hyperoxia-induced oxidative stress. For this purpose, the study analyzed the levels of most relevant oxidative/antioxidative enzymes and DJ-1 protein (protein deglycase DJ-1, also known as Parkinson disease protein 7 [PARK7]) [29], an oxidative stress-sensitive protein which is known to maintain mitochondrial functions by scavenging reactive oxygen species (ROS) [29].…”

Section: Introductionmentioning

confidence: 99%

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Antioxidative effects of uridine in a neonatal rat model of hyperoxic brain injury

Çakır

Koçoğlu

et al. 2020

Turk J Med Sci

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Background/aim: Premature birth is a major problem that results in an increased risk of mortality and morbidity. The management of such infants consists of supraphysiological oxygen therapy, which affects brain development due, in part, to the deterioration caused by reactive oxygen species (ROS). We showed previously that exogenously administered uridine provides neuroprotection in a neonatal rat model of hyperoxic brain injury. Hence, the aim of the present study was to investigate the effects of uridine on ROS in the same setting. Materials and methods: Hyperoxic brain injury was induced by subjecting a total of 53 six-day-old rat pups to 80% oxygen (the hyperoxia group) for a period of 48 h. The pups in the normoxia group continued breathing room air (21% oxygen). Normoxia + saline or hyperoxia + saline or hyperoxia + uridine 100 mg/kg or hyperoxia + uridine 300 mg/kg or hyperoxia + uridine 500 mg/kg was injected intraperitoneally (i. p.) 15 min prior to the hyperoxia procedure. The pups were decapitated and the brains were homogenized to analyze superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), myeloperoxidase (MPO), and malondialdehyde (MDA) enzymes as well as DJ-1 (protein deglycase DJ-1)-an oxidative stress-sensitive protein. Results: Hyperoxia-induced may cause overproduction of oxygen radicals and the oxidant/antioxidant balance may be disturbed in the brain. Brain MPO and MDA levels were significantly increased in saline-receiving pups exposed to hyperoxia. Brain SOD and GSH-Px levels were significantly decreased in saline-receiving pups exposed to hyperoxia. Our results showed that uridine administration prevented the hyperoxia-induced decrease in SOD and GSH-Px while counteracting the hyperoxia-induced increase in MPO and MDA in a dose-dependent manner. Uridine also increased the DJ-1 levels in brains of rat pups subjected to hyperoxia. Conclusion: These data suggest that uridine exhibits antioxidative properties which may mediate the protective effects of uridine in a neonatal rat model of hyperoxic brain injury.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Induction Of Hyperoxic Brain Injurymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Antioxidative effects of uridine in a neonatal rat model of hyperoxic brain injury

Çakır

Koçoğlu

et al. 2020

Turk J Med Sci

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How lung injury and therapeutic oxygen could alter white matter development

Dettman

Dizon

2021

J of Neuroscience Research

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Developmental brain injury describes a spectrum of neurological pathologies resulting from either antenatal or perinatal injury. This includes both cognitive and motor defects that affect patients for their entire lives. Developmental brain injury can be caused by a spectrum of conditions including stroke, perinatal hypoxia‐ischemia, and intracranial hemorrhage. Additional risk factors have been identified including very low birth weight, mechanical ventilation, and oxygen (O2) supplementation. In fact, infants with bronchopulmonary dysplasia, an inflammatory disease associated with disrupted lung development, have been shown to have decreased cerebral white matter and decreased intracranial volumes. Thus, there appears to be a developmental link between the lung, O2, and the brain that leads to proper myelination. Here, we will discuss what is currently known about the link between O2 and myelination and how scientists are exploring mechanisms through which supplemental O2 and/or lung injury can affect brain development. Consideration of a link between the diseased lung and developing brain will allow clinicians to fine tune their approaches in managing preterm lung disease in order to optimize brain health.

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Investigation of the physiological effects of uridine on Nile Tilapia (Oreochromis niloticus)

Zhou,

Ding,

Wang

et al. 2025

Aquaculture

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

Cited by 17 publications

References 45 publications

Antioxidative effects of uridine in a neonatal rat model of hyperoxic brain injury

Antioxidative effects of uridine in a neonatal rat model of hyperoxic brain injury

How lung injury and therapeutic oxygen could alter white matter development

Investigation of the physiological effects of uridine on Nile Tilapia (Oreochromis niloticus)

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