Treatment with a free radical scavenger could be a new option for ischemic brain attack, however, little is known about the alteration of oxidative stress markers induced by edaravone, a novel free radical scavenger, in human ischemic brain attack. Methods:
We investigated the effects of edaravone on the oxidative stress markers in patients with ischemic brain attack. Twentyone patients with ischemic brain attack and 19 controls were enrolled in this study. Blood samples were obtained just before and soon after the first administration of edaravone (30 mg) or ozagrel (40 mg). Intracellular reactive oxygen species of neutrophils were measured using 6carboxy2', 7'dichlorodihydrofluorescin diacetate and a fluorescenceactivated cell sorter. Superoxide from neutrophils, induced by phorbol myristate acetate (PMA), was determined by luminolamplified chemiluminescence assay. Results:
Treatment with 30 mg of edaravone significantly decreased the intracellular reactive oxygen species (ROS) of neutrophils (Wilcoxon test, p=0.0001) and PMAinduced superoxide produced by neutrophils (Wilcoxon test, p=0.001). Ozagrel did not alter the intracellular ROS or superoxide production of neutrophils. Conclusion:
Reduction of intracellular ROS and suppression of superoxide production in neutrophils provide a potential explanation for the clinical efficacy of edaravone in patients with ischemic brain attack.
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