尿苷
神经保护
标记法
脑病
细胞凋亡
医学
生理盐水
麻醉
海马体
内科学
缺氧缺血性脑病
内分泌学
药理学
生物
生物化学
免疫组织化学
核糖核酸
基因
作者
Mehmet Cansev,Zehra Minbay,Bülent Gören,Esra Örenlili Yaylagül,Merih Çetınkaya,Nilgün Köksal,Tülin Alkan
标识
DOI:10.1016/j.neulet.2013.02.035
摘要
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. Rat pups subjected to hypoxic–ischemic insult on postnatal day 7 were injected intraperitoneally with either saline or uridine (100, 300 or 500 mg/kg) for three consecutive days and brains were collected for evaluation of brain infarct volume and apoptosis. Compared with Control group, uridine at 300 and 500 mg/kg doses significantly reduced percent infarct volume, TUNEL(+) cell ratio and active Caspase-3 immunoreactivity in the cortex, as well as in CA1 and CA3 regions of the hippocampus. Uridine (300 and 500 mg/kg) also decreased active Caspase-3 expression in the ipsilateral hemisphere. These data indicate that uridine dose-dependently reduces brain injury in a rat model of neonatal HIE by decreasing apoptosis.
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