Short-term Uridine Treatment Alleviates Endoplasmic Reticulum Stress via Regulating Inflammation and Oxidative Stress in Lithium-Pilocarpine Model of Status Epilepticus.

Background: Status Epilepticus (SE) leads to the development of epilepsy with the contribution of Endoplasmic Reticulum (ER) stress. Uridine, a pyrimidine nucleoside, has been shown to have neuroprotective and antiepileptogenic effects in animal models. This study aimed to determine whether uridine ameliorates ER stress and apoptosis following epileptogenic insult.

Preventive effects of antenatal CDP-choline in a rat model of neonatal hyperoxia-induced lung injury.

Antenatal steroid administration to pregnant women at risk of prematurity provides pulmonary maturation in infants, while it has limited effects on incidence of bronchopulmonary dysplasia (BPD), the clinical expression of hyperoxia-induced lung injury (HILI). Cytidine-5'-diphosphate choline (CDP-choline) was shown to alleviate HILI when administered to newborn rats. Therefore, we investigated effects of maternal administration of CDP-choline, alone or in combination with betamethasone, on lung maturation in neonatal rats subjected to HILI immediately after birth.

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

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.

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

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.

Long-term cognitive effects of uridine treatment in a neonatal rat model of hypoxic-ischemic encephalopathy.

Hypoxic-ischemic encephalopathy (HIE), is the most common brain disorder in neonates during the perinatal period, which, to date, can only be managed to some extent by hypothermia. Uridine is the principal circulating pyrimidine in humans which is utilized as a precursor for membrane phospholipid biosynthesis. Uridine has recently been shown to provide clinical benefit in treatment of Alzheimer's disease due to its involvement in increasing number of brain synapses along with other phospholipid precursors.

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

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.

Neuroprotective effects of uridine in a rat model of neonatal hypoxic-ischemic encephalopathy.

Neonatal hypoxic-ischemic encephalopathy (HIE) is a major cause of neurological disability requiring newer therapeutic strategies. Uridine is the principal circulating pyrimidine in humans and a substrate for nucleotides and membrane phospholipids. The objective of this study was to investigate the effects of uridine in a neonatal rat model of HIE.

Neuroprotective effects of melatonin administered alone or in combination with topiramate in neonatal hypoxic-ischemic rat model.

Purpose: The objective of this study was to compare the effects of two neuroprotective agents; melatonin, a free radical scavenger and topiramate, AMPA/kainate receptor antagonist, administered alone or in combination in neonatal hypoxic-ischemic model.

Methods: After being anesthetized, 7-day-old pups underwent ischemia followed by exposure to hypoxia. The pups were divided into 4 groups in order to receive the vehicle, melatonin, topiramate and combination of topiramate and melatonin.

Possible neuroprotective effects of magnesium sulfate and melatonin as both pre- and post-treatment in a neonatal hypoxic-ischemic rat model.

Background: Perinatal hypoxia-ischemia is a major cause of mortality and long-term neurological deficits.

Objectives: The objective of this study was to compare the effects of two neuroprotective agents; magnesium sulfate and melatonin, administered alone or in combination, on brain infarct volume and TUNEL positivity in a neonatal hypoxic-ischemic (HI) rat model.

Methods: After being anesthetized, 7-day-old pups (n = 80) underwent ischemia followed by exposure to hypoxia for 2 h.

Citicoline and postconditioning provides neuroprotection in a rat model of ischemic spinal cord injury.

Background: Ischemic spinal cord injury is a chain of events caused by the reduction and/or cessation of spinal cord blood flow, which results in neuronal degeneration and loss. Ischemic postconditioning is defined as a series of intermittent interruptions of blood flow in the early phase of reperfusion and has been shown to reduce the infarct size in cerebral ischemia. Our study aimed to characterize the relationship between the neuronal injury-decreasing effects of citicoline and ischemic postconditioning, which were proven to be effective against the apoptotic process.

Neuroprotective effects of postconditioning on lipid peroxidation and apoptosis after focal cerebral ischemia/reperfusion injury in rats.

Aim: Apoptosis after cerebral ischemia/reperfusion (I/R) injury leads to the process of cell death. The deal therapeutic approach would target the apoptosis after I/R. Ischemic postconditioning is a recently discovered neuroprotective strategy that involves the application of brief mechanical reperfusion with a specific algorithm at the onset of reperfusion following an ischemic period.

Neuroproctective effects of ischemic tolerance (preconditioning) and postconditioning.

Elucidation of the endogenous cell survival pathways involved in ischemic tolerance (preconditioning) and postconditioning has significant clinical implications for preventing neuronal damage in susceptible patients. Ischemic tolerance is a phenomenon in which the brain protects itself against future injury by adapting to low doses of noxious insults. Ischemic postconditioning is defined as brief periods of reperfusion alternating with re-occlusion applied during the very early minutes of reperfusion that mechanically alters the hydrodynamics of reperfusion.

Neuronal protective effects of focal ischemic pre- and/or postconditioning on the model of transient focal cerebral ischemia in rats.

We investigated the neuroprotective effects of pre- and postconditioning on infarct volume in the transient middle cerebral artery occlusion (MCAo) model in rats. Thirty-two male rats were divided into occlusion, preconditioning, postconditioning and both pre- and postconditioning groups. MCAo (120 minutes) was monitored with continuous cerebral tissue oxygen (O2) pressure (PtiO2).

Effects of hypoxic preconditioning in antioxidant enzyme activities in hypoxic-ischemic brain damage in immature rats.

Aim: HI (hypoxic-ischemic) brain injury is a major cause of neonatal mortality and longterm neurological morbidity. The aim of the present study was to investigate the effects of HPC (hypoxic preconditioning) on the oxidative-antioxidative status in the neonatal HI brain model.

Material And Methods: Fifty five 7-day-old rats were placed into; Control, HPC, HPC+HI insult, and HI insult groups.

Effects of intranigral vs intrastriatal fetal mesencephalic neural grafts on motor behavior disorders in a rat Parkinson model.

Background: Numerous experimental and clinical studies have shown that intrastriatal fetal mesencephalic grafts grow, survive, and reinnervate host brain tissue, resulting in partial recovery of motor deficits. In addition, pharmacological evidence indicates that these grafts increase dopamine secretion in lesioned brain. However, to date, no grafting method has completely restored the nigrostriatal pathway, and there is no consensus on optimal graft numbers or locations.

Single or multiple small subarachnoid hemorrhages by puncturing a small branch of the rat basilar artery causes chronic cerebral vasospasm.

Objective: This study looked at the effects of single and multiple small subarachnoid hemorrhage (SAH) caused by puncturing a small branch of the basilar artery in rats.

Methods: Rats were subjected to single SAH (n = 21), multiple SAH (n = 21), sham operation (n = 21), or no procedures (control group, n = 7). SAH was induced in rats by transclival puncture of a small branch of the basilar artery.