【摘要】 目的研究Edaravone对视网膜缺血-再灌注损伤(retinal ischem ia-reperfusion injury,RIRI)大鼠视网膜神经节细胞Bc-l2和Bax表达的影响。方法健康Wistar大鼠36只随机分为3组:空白对照组、模型组和Edaravone治疗组。空白对照组不做任何处理,模型组和Edaravone治疗组均采用前房加压法建立大鼠RIRI模型,Edaravone治疗组于缺血前30min行腹腔注射Edaravone(3mg.kg-1),恢复灌注30min后再行腹腔注射Edaravone(3mg.kg-1)。免疫组织化学法检测各组大鼠视网膜缺血-再灌注后24h视网膜神经节细胞Bc-l2和Bax的表达情况。结果空白对照组未见Bc-l2和Bax表达。再灌注后24h,模型组Bc-l2表达为0.406±0.022,Bax表达为0.661±0.034,Bc-l2/Bax为0.609±0.015;Edaravone治疗组Bc-l2表达为0.581±0.031,Bax表达为0.491±0.017,Bc-l2/Bax为1.104±0.094。与模型组比较,Edaravone治疗组Bc-l2表达明显增强(P<0.05),Bax表达明显减弱(P<0.05),Bc-l2/Bax比值升高(P<0.05)。结论 Edaravone对RIRI大鼠视网膜神经节细胞有明显的保护作用,其机制可能与上调Bc-l2表达及下调Bax的表达有关更多还原

【Abstract】 Objective To investigate the effects of edaravone on the expression of Bcl-2 and Bax in retinal ganglion cells of rats with retinal ischemia-reperfusion injury(RIRI).Methods A total of 36 healthy Wistar rats were divided into three groups:the blank control group,the model group and the edaravone treatment group.Rats RIRI model was established in the model group and the edaravone treatment group by elevating intraocular pressure.Intraperitoneal injection of edaravone was then conducted on rats in the edaravone treatment group 30 minutes before retinal ischemia and 30 minutes after retinal ischemia-reperfusion(3 mg·kg-1).Expressions of Bcl-2 and Bax in retinal ganglion cells were detected with immunohistochemical method 24 hours after retinal ischemia-reperfusion.Results No expressions of Bcl-2 and Bax was observed in the blank control group.In the model group,the expression of Bcl-2 and Bax were 0.406±0.022 and 0.661±0.034,respectively,Bcl-2/Bax was 0.609±0.015.In the edaravone treatment group,the expression of Bcl-2 and Bax were 0.581±0.031 and 0.491±0.017 respectively,Bcl-2/Bax was 1.104±0.094.Comparing with the model group,the expression of Bcl-2 in the edaravone treatment group was significantly enhanced while the expression of Bax was weakened,Bcl-2/Bax was increased.Conclusion Edaravone has an protective effect on retinal ganglion cells of rats with RIRI,this mechanism may be associated with its enhancing expression of Bcl-2 and weakening expression of Bax.更多还原