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Goichi Akiyama, Yuriko Azuchi, Xiaoli Guo, Takahiko Noro, Atsuko Kimura, Chikako Harada, Kazuhiko Namekata, Takayuki Harada; Edaravone Prevents Retinal Degeneration in Adult Mice Following Optic Nerve Injury. Invest. Ophthalmol. Vis. Sci. 2017;58(11):4908-4914. doi: 10.1167/iovs.17-22250.
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© ARVO (1962-2015); The Authors (2016-present)
To assess the therapeutic potential of edaravone, a free radical scavenger that is used for the treatment of acute brain infarction and amyotrophic lateral sclerosis, in a mouse model of optic nerve injury (ONI).
Two microliters of edaravone (7.2 mM) or vehicle were injected intraocularly 3 minutes after ONI. Optical coherence tomography, retrograde labeling of retinal ganglion cells (RGCs), histopathology, and immunohistochemical analyses of phosphorylated apoptosis signal-regulating kinase-1 (ASK1) and p38 mitogen-activated protein kinase (MAPK) in the retina were performed after ONI. Reactive oxygen species (ROS) levels were assessed with a CellROX Green Reagent.
Edaravone ameliorated ONI-induced ROS production, RGC death, and inner retinal degeneration. Also, activation of the ASK1-p38 MAPK pathway that induces RGC death following ONI was suppressed with edaravone treatment.
The results of this study suggest that intraocular administration of edaravone may be a useful treatment for posttraumatic complications.
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