Open AccessEdaravone (MCI‐186), a free radical scavenger, attenuates retinal ischemia/reperfusion injury in rats 1
Author(s) -
SONG Yi,
GONG Yuanyuan,
XIE Zhenggao,
LI Caihong,
GU Qing,
WU Xingwei
Publication year - 2008
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2008.00822.x
Subject(s) - edaravone , free radical scavenger , tunel assay , malondialdehyde , retina , retinal , superoxide dismutase , erg , chemistry , oxidative stress , pharmacology , reperfusion injury , retinal ganglion cell , ischemia , apoptosis , medicine , biology , biochemistry , neuroscience
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.