Neuroprotection of edaravone on hypoxic-ischemic brain injury in neonatal rats

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• 作者：Yasuoka ; Noriko ; Nakajima ; Wako ; Ishida ; Akira ; Takada ; Goro
• 关键词：Development and regeneration ; Neuronal death ; Immature brain ; Excitotoxicity ; Mitochondria ; Cytochrome c ; Caspase-3 ; Neuronal cell death
• 刊名：Developmental Brain Research
• 出版年：2004
• 出版时间：July 19, 2004
• 年：2004
• 卷：151
• 期：1-2
• 页码：129-139
• 全文大小：1.03 M

文摘

Edaravone has an inhibitory effect on lipid peroxidation by scavenging free radicals and prevents vascular endothelial cell injury. We examined whether edaravone was effective on hypoxic-ischemic (HI) brain injury in immature brain or not using the Rice-Vannucci model. The initial dose, 3 mg/kg (0.05 ml) of edaravone, was injected intraperitoneally just before hypoxic exposure. Subsequently, the same dose was injected every 12 h until the animals were killed. Controls received saline injection as the same protocol. Macroscopic evaluation of brain injury revealed that the neuroprotective effect of edaravone on HI brain after 48 h post HI. TUNEL showed that edaravone injection decreased neurodegeneration. Quantitative analysis of cell death using H&E-stained 2.5 μm sections showed that there was a trend for both necrotic and apoptotic cells to decrease in edaravone injection group. Edaravone injection inhibited the release of cytochrome c from mitochondria to cytosol and caspase-3 activation in cortex and hippocampus between 24 and 168 h post HI. Our results suggest that edaravone is protective after HI insult in the immature brain by decreasing both apoptosis and necrosis and also by inhibiting mitochondrial injury.