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. 2010 Apr;107(4):347-53.
doi: 10.1007/s00347-009-2030-1.

[Erythropoietin protects retinal ganglion cells and visual function after ocular ischemia and optic nerve compression]

[Article in German]
T Jehle  1 , W Meschede, R Dersch, N Feltgen, M Bach, W A Lagrèze
Affiliations

[Erythropoietin protects retinal ganglion cells and visual function after ocular ischemia and optic nerve compression]

[Article in German]
T Jehle et al. Ophthalmologe. 2010 Apr.

Abstract

Background: The glycoprotein erythropoietin (EPO) has been shown to be protective in models of neuronal disease and reduced apoptosis of retinal ganglion cells (RGC) after transection of the optic nerve and in glaucoma. In this study we assessed in vivo the properties of EPO on survival of RGC after ischemia and optic nerve compression, as well as on postischemic visual function. Furthermore, the safety of intravitreal injection was assessed.

Methods: In all experiments, EPO was administered intravitreally in male Brown Norway rats. Ocular ischemia was induced by elevating the intraocular pressure for 55 min. The calibrated optic nerve compression was performed for 10 s. RGC were marked stereotactically and quantified by fluorescence microscopy. The retinal function was quantified by electroretinography (ERG) and the whole visual pathway by visual evoked potential (VEP).

Results: EPO (2 and 20 units per eye, n=9-21) increased the survival of RGC after ischemia by 21+/-21% and 127+/-31% (mean +/- SEM) and after optic nerve compression by 28+/-12% and 58+/-13%. With EPO (20 units), postischemic function was increased, in ERG by 71+/-13% (a-wave) and 75+/-19% (b-wave) and in VEP by 264+/-65% (p=0.053). Neither the ERG parameters, nor the VEP, nor the number of RGC differed significantly after intravitreal injection of EPO (5, 50, and 200 units, n=6-7) in healthy eyes.

Conclusion: The combination of toxicological safety and protection of retinal neurons makes EPO a promising drug for ischemic retinal diseases and traumatic optic neuropathy.

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References

    1. Invest Ophthalmol Vis Sci. 2008 Feb;49(2):732-42 - PubMed
    1. Graefes Arch Clin Exp Ophthalmol. 2008 Sep;246(9):1255-63 - PubMed
    1. Naunyn Schmiedebergs Arch Pharmacol. 2000 Jul;362(1):74-81 - PubMed
    1. Invest Ophthalmol Vis Sci. 2007 Mar;48(3):1212-8 - PubMed
    1. Br J Ophthalmol. 2009 Dec;93(12):1667-71 - PubMed

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