Abstract
Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, is used for the clinical treatment of retinal injury. In this study, we investigated the protective effects of edaravone against diabetic retinal damage in the mouse. Diabetic retinopathy in the mouse was induced by injection of streptozotocin. Edaravone was given once-daily and was intraperitoneally (i.p.) treated at a dose of 3 mg/kg from streptozotocin injection to 4 weeks after onset of diabetes. Retinal ganglion cells (RGCs) damage was evaluated by recording the pattern electroretinogram (ERG). RGCs damage was also detected by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and the levels of reactive oxygen species (ROS) were determined fluorometrically. The expressions of phosporylated-ERK1/2, BDNF, and caspase-3 were determined by Western blot analysis. Retinal levels of ROS, phosphorylated ERK1/2, and cleaved caspase-3 were significantly increased, whereas the expression of BDNF was significantly decreased in the retinas of diabetic mice, compared to nondiabetic mice. Administration of edaravone significantly attenuated diabetes induced RGCs death, upregulation of ROS, ERK1/2 phosphorylation, and cleaved caspase-3 and downregulation of BDNF. These findings suggest that oxidative stress plays a pivotal role in diabetic retinal damage and that systemic administration of edaravone may slow the progression of retinal neuropathy induced by diabetes.
Highlights
Diabetes produces a spectrum of retinal abnormalities that result in damage to the vasculature and neurons, and in severe cases, loss of vision itself
To investigate the role of oxidative stress in retinal damage after diabetes, we focused on the effects of edaravone, a free radical scavenger, against retinal damage by diabetes-induced retinopathy
In our rodent model of diabetic retinal neuropathy, we found evidence of a substantial increase in oxidative stress
Summary
Diabetes produces a spectrum of retinal abnormalities that result in damage to the vasculature and neurons, and in severe cases, loss of vision itself. Achievement and maintenance of glycemic control has been difficult or impossible in many patients, effective therapies are needed to inhibit the retinopathy. Recent studies have shown that the retina has a high content of polyunsaturated fatty acids and has the highest oxygen uptake and glucose oxidation relative to any other tissue. This phenomenon renders retina more susceptible to oxidative stress [2]. Oxidative stress, which may occur because of an imbalance between the production and removal of reactive oxygen species (ROS), is considered to be a critical mediator in RGC injury of various etiologies and has been implicated in RGC death in the diabetic retinopathy
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