Tanaka Masahiko
Pharmaceuticals Development Division, Mitsubishi Pharma Corporation, 2-2-6 Nihonbashi-Honcho, Chuo-ku, Tokyo 103-8405, Japan.
Nihon Yakurigaku Zasshi. 2002 May;119(5):301-8. doi: 10.1254/fpj.119.301.
The involvement of oxygen radical species has been implicated in ischemic and post-ischemic brain cell damage. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one; M.W. 174.20, MCI-186, Radicut Injection) has an inhibitory effect on lipid peroxidation by scavenging free radicals and prevents vascular endothelial cell injury. In rat brain ischemic models, post-ischemic treatment with edaravone reduces .OH production and infarction of the ischemic penumbral area and suppresses delayed neuronal death. It also improves neurological deficits and diminishes deterioration of brain edema observed after ischemia. We investigated the efficacy and safety of edaravone in acute ischemic stroke patients. Edaravone improved the core neurological deficits, impaired activities of daily living, and disability, without serious safety problems. Edaravone was approved in Japan for the treatment of acute brain infarction within 24 h after onset in April, 2001. We hope that edaravone represents a promising neuroprotective agent that can contribute to the treatment of acute ischemic stroke.
氧自由基参与了缺血性和缺血后脑细胞损伤。依达拉奉(3-甲基-1-苯基-2-吡唑啉-5-酮;分子量174.20,MCI-186,必存注射液)通过清除自由基对脂质过氧化具有抑制作用,并可防止血管内皮细胞损伤。在大鼠脑缺血模型中,缺血后给予依达拉奉可减少·OH生成,减轻缺血半暗带区域的梗死,并抑制迟发性神经元死亡。它还可改善神经功能缺损,减轻缺血后观察到的脑水肿恶化。我们研究了依达拉奉在急性缺血性脑卒中患者中的疗效和安全性。依达拉奉改善了核心神经功能缺损、受损的日常生活活动能力和残疾状况,且无严重安全问题。2001年4月,依达拉奉在日本被批准用于治疗发病24小时内的急性脑梗死。我们希望依达拉奉是一种有前景的神经保护剂,可有助于急性缺血性脑卒中的治疗。