背景 随着糖尿病患者数量的增加,糖尿病角膜病变越来越受到人们的重视,导致糖尿病角膜病变发病的主要原因为糖尿病引起的角膜神经病变,探讨糖尿病角膜神经病变的具体发病机制具有重要意义.目的探讨新型自由基清除剂依达拉奉对糖尿病大鼠角膜神经病变的保护作用,研究氧化应激在糖尿病角膜神经病变发病机制中的作用.方法健康雄性SD大鼠70只,其中20只不做任何处理作为正常对照组；其余50只采用一次性腹腔注射链脲佐菌素(STZ) (60 mg/kg)诱导建立糖尿病大鼠模型,成模后选取血糖＞15 mmol/L的40只大鼠应用随机数字表法随机分为依达拉奉治疗组和糖尿病对照组,依达拉奉治疗组及糖尿病对照组每天分别给予自制的0.2 g/L依达拉奉滴眼液及生理盐水点眼,每次1滴,每日3次,预防性用药直至实验动物被处死.分别于造模成功后的第6、8、10、12周每组处死5只大鼠,观察角膜知觉、角膜神经形态、角膜神经纤维数量、角膜组织中丙二醛含量及超氧化物歧化酶(SOD)活性.结果糖尿病对照组自造模第6周起大鼠角膜知觉下降、角膜神经纤维数量减少、神经网丛密度稀疏、神经分支变细、神经活性降低,角膜组织中丙二醛含量明显增多,SOD活性明显下降(P＜0.01).随着病程的延长,上述变化日益明显.依达拉奉治疗组与糖尿病对照组比较,角膜知觉有所提高,神经形态学明显改善,至第12周时尚存有部分分支,角膜组织中丙二醛含量明显减少,SOD活性显著提高(P＜0.01). 结论依达拉奉可降低糖尿病角膜神经病变所致的角膜神经损伤,氧化应激可能为糖尿病角膜神经病变的重要发病机制.%Background With the number of diabetics increases,people pay more attention to the diabetic keratopathy.The major mechanism leading to diabetic keratopathy is diabetic corneal neuropathy.So it is significant to observe pathologic mechanism of diabetic corneal neuropathy. Objective To investigate the protective effects of edaravone( a free radical scavenger) on corneal nerve of rats with experimental diabetic corneal neuropathy,then explain the effects of oxidative stress in the pathologic mechanism of diabetic corneal neuropathy. Methods Seventy Sprague-Daxley male rats were taken as experimental subjects and 20 of them were used as normal control group.The remaining 50 were induced to be diabetic mellitus by a single intraperitoneal injection of streptozotocin and divided into 2 groups randomly:edaravone treated group and diabetic control group.In the edaravone treated group,edaravone(0.2 g/L) eye drops were used 3 times a day until the animal was killed.Five rats in each group were sacrificed at 6,8,10 and 12 weeks respectively.Then the corneal sensation,number of corneal nerve fibers,morphology,content of malondialdehyde(MDA) and activity of superoxide dismutase(SOD) in the corneal tissue were detected. Results In the diabetic control group,the corneal sensation and the number of corneal nerve fibers were decreased,the density of neural network for cluster was sparse,the nerve activity was decreased,the content of MDA in the corneal tissue was significantly increased,the activity of SOD in the corneal tissue was significantly decreased (P＜0.01 ).Accompany with the course of disease,the above change was obvious day after day.Compared with the diabetic control group,the corneal sensation and the morphological abnormalities in corneal nerve of edaravone group were improved significantly which had the partial branches to the 12th week,the content of MDA in the corneal tissue was significantly decreased,the activity of SOD in the corneal tissue was significantly increased (P＜0.01).Conclusions Edaravone can lower diabetic corneal nerve of rats with experimental diabetic corneal neuropathyinjury,Oxidative stress may be a critical pathologic mechanism of diabetic corneal neuropathy.
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