依达拉奉对颅眶联合伤后视网膜神经节细胞的保护作用

Protective effects of edaravone on the retinal ganglion cells after cranio-orbital injury in rats

目的探讨实验性大鼠颅眶联合伤(cranio-orbital injury,COI)后视网膜神经节细胞(retinal ganglion cells,RGC)凋亡机制及依达拉奉的保护作用。方法 144只清洁级SD大鼠,随机分为对照组(n=48)、损伤组(n=48)和治疗组(n=48),建立颅眶联合伤模型后,治疗组给予依达拉奉(30 mg/kg)干预治疗,损伤组不做处理。伤后3、6、10、14 d,检测三组大鼠伤侧眼球RGC活性氧(reactive oxygen species,ROS)含量及凋亡率,并观察凋亡RGC形态和超微结构。结果损伤组RGC的ROS含量伤后6、10、14 d明显高于治疗组和对照组(P<0.05)。伤后3、6、10、14 d,损伤组RGC凋亡率显著高于对照组及治疗组(P<0.05)。损伤组RGC的微观及超微结构均表现出典型的凋亡特征,对照组和治疗组RGC多为正常。结论 COI后RGC的ROS含量明显升高,导致凋亡失衡。依达拉奉通过清除ROS阻止这一病理过程,具有明确的视神经保护作用,值得临床推广。

Objective To investigate the mechanism of apoptosis in retinal ganglion cells（RGC） and protective effects of edaravone on rats after experimental cranio-orbital injury（COI）. Methods A total of 144 rats（Sprague Dawley, clean grade） were randomly divided into control group（n = 48）, injury group（n = 48） and treatment group（n = 48）. The COI model was established and edaravone（30 mg/kg） was injected intraperitoneally to rats in treatment group for intervention therapy and no intervention was performed in rats in injury group. The content of reactive oxygen species（ROS） and apoptosis rate of RGC were detected 3, 6, 10, 14 d after COI. The morphology and ultrastructure of apoptosis RGC were also observed. Results The content of ROS in RGC in injury group was higher than that in treatment and control groups 6, 10 and 14 d after COI（P〈0.05）. The apoptosis rate of RGC in injury group was higher than that in treatment and control groups 3, 6, 10, 14 d after COI（P〈0.05）. The microstructure and ultrastructure of RGC showed the typical characteristics of apoptosis in injury group but appeared normal in treatment and control groups. Conclusions The content of ROS in RGC could increase significantly after COI, which results in apoptosis imbalance in RGC. Edaravone can prevent this pathological process by eliminating ROS, and thus having a protective effect on optic nerve and is worthy to be popularized clinically.