Abstract
Abstract Purpose: Purpose:EPO is approved drug for anaemia treatment. Its antiapoptotic effects in animal models of glaucoma and retinal degeneration, when administered systemic or intravitreous are known. It provides neuroprotection and avoids cell damage in diabetic rats. It is upregulated in the retina in proliferative diabetic retinopathy (PDR). We studied serum EPO expression in diabetics and in normal non diabetic controls. Methods: Methods:In 58 type 2 diabetics, 24 with and 34 without retinopathy, of both sexes aged 64.24±11.64 years, EPO serum expression was determined by ELISA and compared to 44 non diabetic controls age and sex matched. Statistical analyses was applied (Χ2, Student t test). Results: Results:Serum EPO expression was highest in diabetics with retinopathy (15.15±11.44 mIu/ml, high in diabetics without retinopathy, 10.084±6.63 p=0.043), compared to the controls 9.47±6.57. Conclusions: Conclusions:EPO serum upregulation in diabetic retinopathy supports endogenous over production seen in the retina with PDR. High EPO expression could be an attempt of nature’s protective mechanism. Human recombinant EPO is known to protect retinal neurones in various animal models of stress: ischemia/reperfusion/ocular hypertension/glaucoma (rats, mice, rabbits). EPO administration to RCS rats appears to exert (in vivo) neuroprotective effect on the photoreceptors. HrEPO may be necessary to protect the damage of retinal tissue in diabetics. Constitutional EPO seems to be insufficient to give effective protection in diabetic retinopathy. Thus EPO could be an important therapeutic target molecule for the survival of damaging retinal cells.
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