AIM: To investigate the effect of edaravone (MCI-186), a free radical scavenger, against ischemia/reperfusion (I/R) injury in the rat retina. METHODS: Retinal ischemia was induced in male Sprague-Dawley rats by elevating intraocular pressure to 110 mmHg for 60 min. The rats were intraperitoneally injected with edaravone at a dose of 3 mg/kg at 30 min before ischemia, and then treated with edaravone (3 mg/kg, ip) twice daily for 1 or 5 d after I/R. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the retinal tissues were determined on d 1 after I/R injury. The apoptosis of retinal neurons was detected on d 1 after I/R injury by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling staining. The electroretinogram (ERG) was recorded on d 5 after reperfusion. RESULTS: Edaravone lowered MDA levels, raised SOD activity, and attenuated I/R-induced apoptosis of retinal neurons within the inner nuclear, ganglion cell, and outer nuclear layers of the rat retina. Moreover, edaravone suppressed I/R-induced reduction in a- and b-wave amplitudes of ERG. CONCLUSION: Edaravone can protect the retina from I/R injury in rats through reducing oxidative stress and inhibiting apoptosis of retinal neurons, which suggests that edaravone might be a potential choice for the treatment of I/R-induced eye disorders.
AIM: To investigate the effect of edaravone (MCI-186), a free radical scavenger, against ischemia/reperfusion (I/R) injury in the rat retina. METHODS:Retinal ischemia was induced in male Sprague-Dawley rats by elevating intraocular pressure to 110 mmHg for 60 min. The rats were intraperitoneally injected with edaravone at a dose of 3 mg/kg at 30 min before ischemia, and then treated with edaravone (3 mg/kg, ip) twice daily for 1 or 5 d after I/R. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the retinal tissues were determined on d 1 after I/R injury. The apoptosis of retinal neurons was detected on d 1 after I/R injury by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling staining. The electroretinogram (ERG) was recorded on d 5 after reperfusion. RESULTS:Edaravone lowered MDA levels, raised SOD activity, and attenuated I/R-induced apoptosis of retinal neurons within the inner nuclear, ganglion cell, and outer nuclear layers of the rat retina. Moreover, edaravone suppressed I/R-induced reduction in a- and b-wave amplitudes of ERG. CONCLUSION:Edaravone can protect the retina from I/R injury in rats through reducing oxidative stress and inhibiting apoptosis of retinal neurons, which suggests that edaravone might be a potential choice for the treatment of I/R-induced eye disorders.