Song Yi, Gong Yuan-yuan, Xie Zheng-gao, Li Cai-hong, Gu Qing, Wu Xing-wei
Ophthalmic Center, Shanghai Jiaotong University, Shanghai 200080, China.
Acta Pharmacol Sin. 2008 Jul;29(7):823-8. doi: 10.1111/j.1745-7254.2008.00822.x.
To investigate the effect of edaravone (MCI-186), a free radical scavenger, against ischemia/reperfusion (I/R) injury in the rat retina.
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.
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.
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.
研究自由基清除剂依达拉奉（MCI-186）对大鼠视网膜缺血/再灌注（I/R）损伤的作用。
通过将雄性Sprague-Dawley大鼠眼压升高至110 mmHg持续60分钟诱导视网膜缺血。在缺血前30分钟，给大鼠腹腔注射3 mg/kg剂量的依达拉奉，然后在I/R后每天两次腹腔注射依达拉奉（3 mg/kg），持续1或5天。在I/R损伤后第1天测定视网膜组织中丙二醛（MDA）和超氧化物歧化酶（SOD）的水平。在I/R损伤后第1天通过末端脱氧核苷酸转移酶介导的地高辛-dUTP缺口末端标记染色检测视网膜神经元的凋亡。在再灌注后第5天记录视网膜电图（ERG）。
依达拉奉降低了MDA水平，提高了SOD活性，并减轻了大鼠视网膜内核层、神经节细胞层和外核层中I/R诱导的视网膜神经元凋亡。此外，依达拉奉抑制了I/R诱导的ERG a波和b波振幅降低。
依达拉奉可通过减轻氧化应激和抑制视网膜神经元凋亡来保护大鼠视网膜免受I/R损伤，这表明依达拉奉可能是治疗I/R诱导的眼部疾病的潜在选择。
