Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

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Neonatal hypoxic-ischemic encephalopathy (HIE) is the most frequent neurologic disease in the perinatal period. Its major cause is oxidative stress, which induces DNA peroxidation and apoptotic neuronal death. We examined 8-hydroxy-2′-deoxyguanosine (8-OHdG) expression to evaluate brain damage in neonatal HIE and the therapeutic effect of edaravone, a free radical scavenger. Using HPLC and immunohistochemistry, the 8-OHdG levels of neonatal HIE model Sprague-Dawley rats that were subjected to left common carotid artery ligation and 2-h hypoxia significantly increased after 24–48 h of hypoxic-ischemic (HI) insult, but decreased after 72 h. Moreover, the number of apoptotic cells with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and karyorrhexis significantly increased after 24–72 h of HI insult. In a therapeutic experiment, edaravone was administered i.p. (9 mg/kg) after HI insult every 24 h. Edaravone reduced both the apoptotic neuronal cell number and 8-OHdG expression after 24–48 h of HI. From a double immunofluorescent study, DNA peroxidation occurred in apoptotic neuronal cells with 8-OHdG expression. Edaravone may inhibit the number of apoptotic neuronal cells and 8-OHdG expression within 48 h after HI insult.

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