• Neuropharmacology · Feb 2005

    Comparative Study

    The radical scavenger edaravone prevents oxidative neurotoxicity induced by peroxynitrite and activated microglia.

    • Masahiro Banno, Tetsuya Mizuno, Hideki Kato, Guiqin Zhang, Jun Kawanokuchi, Jinyan Wang, Reiko Kuno, Shijie Jin, Hideyuki Takeuchi, and Akio Suzumura.
    • Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa, Nagoya 464-8601, Japan.
    • Neuropharmacology. 2005 Feb 1;48(2):283-90.

    AbstractThe free radical scavenger edaravone has been used as an anti-oxidative agent in acute ischemic brain disorders. We examined the effect of edaravone on the production of nitric oxide (NO), reactive oxygen species (ROS) and proinflammatory cytokines by activated microglia, and we also examined its neuroprotective role in cortical neuronal cultures oxidatively stressed by the peroxynitrite donor N-morpholinosydnonimine (SIN-1) or activated microglia. Edaravone significantly suppressed the production of NO and ROS by activated microglia, though it did not suppress production of inflammatory cytokines. In addition, edaravone significantly suppressed neuronal cell death and dendrotoxicity induced by either SIN-1 or activated microglia in a dose-dependent manner. These results suggest that edaravone may function as a neuroprotective agent counteracting oxidative neurotoxicity arising from activated microglia, as occurs in either inflammatory or neurodegenerative disorders of the central nervous system.

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